Content uploaded by Gabriel Paz
Author content
All content in this area was uploaded by Gabriel Paz on Sep 07, 2014
Content may be subject to copyright.
EFFECTS OF DIFFERENT ANTAGONIST PROTOCOLS ON
REPETITION PERFORMANCE AND MUSCLE ACTIVATION
– ORGINAL RESEARCH
Gabriel A. Paz1(A,C,D,E,F), Jeffrey M. Willardson2 (D,E), Roberto Simão1 (A, C, D), Humberto Miranda1 (A, C, D, E)
1Universidade Federal do Rio de Janeiro, School of Physical Education and Sports, Rio de Janeiro, RJ, Brazil
2Kinesiology and Sports Studies Department, Eastern Illinois University, Charleston, IL, USA
Abstract
Objective: To investigate the acute effects of different antagonist manipulation protocols on maximal repetition perfor-
mance and muscle activation during seated row (SR) exercise.
Methods: Fifteen men (22.4 ± 1.1 years old, height 175 cm ± 5.5, weight 76.6 kg ± 7, and 12.3 ± 2.1 of body fat per-
centage) with previous resistance training experience (3.5 ± 1.2 years) performed four experimental protocols: (TP) one
set to repetition failure of SR exercise; (AS) Antagonist static stretching for the pectoralis major (PM) followed by one set
of SR; (PNFA) Proprioceptive neuromuscular facilitation for PM followed by one set of the SR; (APS) One set of the bench
press with a 10 RM loads followed by one set of the SR. The maximal repetitions and the electromyographic (EMG) signal
were recorded for the latissimus dorsi (LD), biceps brachii (BB), triceps brachii lateral head (TL), and PM during the SR.
Results: A significant increase in SR repetition performance was noted for the APS (14 ± 1) versus the TP (9 ± 1.2, P
= 0.0001), PNFA (10 ± 1.5, P = 0.001), and AS (12 ± 1.5, P = 0.004) protocols. A significant increase in SR repetitions was
also noted for the AS versus the TP (P = 0.001) and PNFA (P = 0.002) protocols. The muscle activation of the BB and LD
were significantly higher during the APS and AS versus the PNFA and TP sessions.
Conclusions: These results suggest that either using the APS or AS approaches can facilitate an increase in SR repeti-
tion performance versus traditional resistance exercise sets.
Keywords: paired set, strength, stretching, coactivation, performance
Introduction
Resistance training (RT) provides an overload to the
musculoskeletal system, leading to an increase in muscle
strength [1]. In formulating aRT prescription, it is of
the utmost importance to understand the interaction
among training variables such as the load, volume, num-
ber of exercises, number of repetitions per set, exercise
order, number of sets per exercise or muscle group, and
the rest interval between sets and exercises [2].
Most functional movements and RT exercises
involve some activation of the antagonist muscles in
conjunction with activation of the agonist muscles [3].
This phenomenon has been described as coactivation
or co-contraction and affects the net joint torque and
subsequent movement velocity [4]. Greater activation
of the antagonists during amovement produces abrak-
ing effect for the agonists in the mechanical expression
of force and power [5,6]. Prior studies have incorpo-
rated pre-stretching or pre-fatiguing of the antagonist
musculature to facilitate the action of the agonists
during subsequent movements [7,8]. The stretching
or pre-loading of the antagonist musculature may
promote neural inhibition of these muscle groups,
lowering the ratio of agonist/antagonist coactivation
[9], and consequently increasing rotary torque for the
agonist musculature [10,11].
One method for achieving antagonist pre-loading
during RT is to perform aset for the antagonist mus-
culature immediately prior to aset for the agonist
musculature. This model of pre-loading has been
referred to as “agonist-antagonist paired set training
(APS)” [9]. During APS training, agonist and antago-
nist muscles are trained “back-to-back”, with limited
or without rest between paired sets [12]. However,
there is insufficient evidence to support this hypoth-
esis, since some authors found deleterious effects on
force production of the agonists [11] or observed no
changes in the electromyographic (EMG) amplitude
normalized by percentage of maximal voluntary
contraction of antagonist muscles following different
manipulation protocols such as pre-loading or static
stretching [5,13,14].
Despite the lack of evidences about the potential
training effects of antagonist manipulation protocols,
multiple studies with varying methodologies have
investigated different aspects of manipulating the
antagonist musculature on subsequent movement
performance; these have included the application of
static stretching of the antagonists during warm-up
[7,8], comparison between different types of muscle
action (eccentric, concentric, isometric) [15,16], and
velocities [10,13]. However, few studies have reported
Medicina Sportiva
Med Sport 17 (3): 106-112, 2013
DOI: 10.5604/17342260.1068221
Copyright © 2013 Medicina Sportiva
ORIGINAL RESEARCH
106
107
Paz G.A., Willardson J.M., Simão R., Miranda H. / Medicina Sportiva 17 (3): 106-112, 2013
EMG data for the agonist/antagonist musculature dur-
ing movements preceded by antagonist manipulation
[3,7,8,17].
Further study is warranted on the practical implica-
tions of manipulating the antagonist musculature in
different ways for acute enhancement of agonist per-
formance that may in turn positively affect longitudi-
nal training outcomes. Additionally, RT protocols that
improve acute performance could be atime efficient
alternative for coaches and practitioners aiming to
optimize the quality of exercise sessions and outcomes.
Therefore, the purpose of this study was to investigate
the acute effects of manipulating the antagonist mus-
culature via performance of the bench press, static
stretching and proprioceptive neuromuscular facili-
tation stretching for pectoralis major on subsequent
maximal repetition performance and muscle activa-
tion for the agonist/antagonist muscles during awide
grip seated row (SR) exercise in trained men.
Methods
Participants
Fifteen recreationally trained men participated as
subjects in this study (22.4 ± 1.1 years old, height 175
cm ± 5.5, weight 76.6 kg ± 7, and 12.3 ± 2.1 of body
fat percentage). All subjects had previous RT experi-
ence (3.5 ± 1.2 years), with amean frequency of four
60-minute sessions per week, using 1- to 2-minute
rest intervals between sets and exercises. All subjects
completed the Physical Activity Readiness Question-
naire (PAR-Q) and signed an informed consent before
participation in this study according to the Declaration
of Helsinki. Subjects were encouraged to report for
workout sessions fully hydrated and to be consistent in
their food intake throughout the duration of the study;
and asked to refrain from any upper-body training in
the 48 hours prior to each workout session. The study
was approved by the university’s ethic committee.
Experimental Protocols
This study used arandomized crossover design
during which subjects performed four experimental
protocols. The protocols were preceded by two testing
sessions during which the 10 repetition maximum
(RM) was assessed for the bench press (BP) and SR
exercises. The four experimental protocols were then
instituted on non consecutive days and 72 hours apart
in random order and included: 1) Traditional Protocol
(TP) - one set to repetition failure of the SR exercise; 2)
Antagonist Stretching (AS) - one set of static stretching
(40 s) for the pectoralis major followed by one set of
the SR; 3) Antagonist Proprioceptive Neuromuscular
Facilitation (PNFA) stretching for the pectoralis major
followed by one set of the SR; 4) Antagonist paired
set (APS) - one set of the BP to repetition failure fol-
lowed by one set of the SR. The AS protocol involved
one set of 40 seconds of static stretching for the pec-
toralis major (PM) muscle followed by one set of the
SR exercise. The PNFA protocol involved one set of
40 seconds (20 seconds of isometric tension and 20
seconds of passive stretch) of the contract-relax PNF
stretching technique for the PM, followed by one set of
the SR exercise. No rest interval was allowed between
antagonist manipulation and the ensuing SR exercise.
Dependent variables included the number of repeti-
tions completed and root mean square (RMS) EMG
signal for the latissimus dorsi (LD), biceps brachii
(BB), triceps braquii lateral head (TL) and pectoralis
major (PM) during the SR.
10 Repetition Maximum Testing
In the week prior to performance of the first
randomly selected protocol, 10RM loads were tested
and re-tested in two sessions for each subject in the
BP and the SR (Life Fitness, IL, USA) exercises (Fig.
1). The 10RM was defined as the maximum weight
that could be lifted for 10 consecutive repetitions
at aconstant velocity of 4 seconds per repetition (2
seconds for the concentric phase and 2 seconds for
the eccentric phase) [8]. The execution of the BP and
SR were standardized and pauses were not permitted
between the concentric and eccentric phases (Fig. 2).
Ametronome (Metronome Plus, M&M System Ger-
many, version 2.0) was used to help control the lifting
Fig 1. Summary for experimental protocol trials
108
Paz G.A., Willardson J.M., Simão R., Miranda H. / Medicina Sportiva 17 (3): 106-112, 2013
cadence. However, if subjects slowed their cadence due
to fatigue, all completed repetitions were still counted.
If a10RM was not accomplished on the first attempt,
the weight was adjusted by 4–10 kg and aminimum
5-minute rest was permitted before the next attempt.
Only three trials were allowed per testing session. The
test and retest trials were conducted on different days
with aminimum of 48 hours between tests.
Stretching Exercises
The static and PNF stretches applied to the PM
muscle were consistent with the protocol previously
conducted by Franco et al. [20]. Subjects maintained
astanding position, preserving the physiological
curvature of the spine; the researcher then instituted
apassive stretch for the PM via horizontal abduction
of the shoulder joints with the elbow joints fully flexed.
According to Franco et al. [20], 40 s of static or PNF type
stretching induced significant reductions in the force
production and activation of the stretched muscles.
Electromyographic acquisition and analysis
The EMG data of LD, BB, PM, and TL muscles were
evaluated during the SR exercise. Before the placement
of the electrodes, the areas were shaved and cleaned
with alcohol until aslight redness was apparent [21].
The PM electrode was placed at the midpoint between
the acromion process and the xiphoid process. The LD
electrode was placed lateral to the inferior angle of the
scapula. The BB electrode was placed on the line be-
tween the medial acromion and the cubit fossa. The TL
electrode was placed half way between the acromion
process and the olecranon process at 2 finger widths
below the medial line [22].
The EMG data were captured through passive bi-
polar surface electrodes (Kendal Medi Trace 200, Tyco
Healthcare, Pointe-Claire, Canada) with recording di-
ameter = 1 mm and distance between electrode center
= 1 cm. The surface electrodes were placed over the
muscles bellies. The electrodes were connected to an
analog to digital converter of 16 bits (EMG System of
Brazil, Sao Jose dos Campos, SP, Brazil) and acquired
with the assistance of proprietary software (EMGlab,
EMG System of Brazil, Sao Jose dos Campos, SP, Bra-
zil). The EMG signals were amplified by 1.000 with
acommon mode rejection ratio of 100dB. The signal
was sampled at 1000 Hz and 4th order Butterworth
filter was applied in forward and reverse direction. The
reference electrode was placed on the clavicle bone.
Apermanent marker was used to mark the location
of the electrodes during the first testing session for
consistent electrode placement during subsequent
sessions [21]. The impedance between electrode pairs
was less than 5 kΩ using a25-Hz signal through the
electrodes [21]. All these procedures were performed
by the same investigator.
The criterion used for normalization of the EMG
activity was the MVIC. Three MVICs were performed
against afixed resistance in the following positions as
proposed by Kendall et al. [23]. The isometric action
was maintained for 10 seconds with 20 second rest in-
tervals between the three actions for each muscle. For
the MVICs, analyses was conducted within awindow
of 4 seconds between the second and sixth seconds
of contraction. The highest RMS value of the three
MVICs was used for normalization [24]. The mean
amplitude of the RMS was performed using the cus-
tom-written software Matlab 5.02c (MathworksTM,
Natick, USA). The averaging window for RMS was
100 ms and all reported values are the mean RMS over
apredetermined sampling window from the onset to
the end of each contraction. EMG data was collected
for the entire (concentric and eccentric phases) SR set
for each protocol. EMG data was expressed as percent-
age relative to the largest RMS value of the EMG signal
obtained for the MVIC (100%) [18,19].
Fig. 2. Resistance exercises bench press (a) and wide grip seated row (b)
109
Paz G.A., Willardson J.M., Simão R., Miranda H. / Medicina Sportiva 17 (3): 106-112, 2013
Statistical analysis
The 10-RM test–retest reliability was calculated
through the intraclass correlation coefficient (ICC =
(MSb – MSw)/[MSb + (k-1)MSw)]), where MSb = mean-
square between, MSw = means-square within, and k =
average group size. The normality and homoscedastic-
ity of the data was analyzed via the Shapiro-Wilk test
and Bartlett test of Sphericity (P = 0.167); subsequently,
all variables presented normal distribution and ho-
moscedasticity. Aone-way ANOVA with repeated-
measures was used to assess differences in repetition
performance between experimental protocols and
muscle activation during the SR exercise. Significant
main effects were further assessed using Bonferroni
post hoc test. Aprobability value of P < 0.05 was used
to establish the significance of all comparisons. Statis-
tical analysis was performed with the SPSS software
version 20.0 (Chicago, IL, USA).
Results
The 10RM loads for BP and SR exercise were 85 ±
10.1 kg and 70.2 ± 12,3 kg, respectively. The ICCs for
the 10RM tests were as follows: SR = 0.95 and BP =
0.92. The total repetitions completed for the SR under
the TP, AS, PNFA, and APS protocols are presented in
Fig. 3. Significant increases on repetition performance
for SR exercise were noted for APS versus the TP (P =
0.0001), PNFA (P = 0.001) and AS (P = 0.004) condi-
tions. Furthermore, ahigher number of SR repetitions
were also found for AS versus the TP (P = 0.001) and
PNFA (P = 0.002), respectively. No significant differ-
ences were noted between the PNFA and TP.
Significant increase on LD activity was noted for
APS versus the TP (P = 0.0001) and PNFA (P = 0.002)
protocols; significantly greater LD activation was also
found for AS compared to TP (P = 0.001) and PNFA
(P = 0.003). Similarly, BB muscle activation was higher
Fig. 3. Mean + SD repetitions for the SR exercise under antagonist manipulation protocols; SR: seated row; TP: traditional protocol; PNFA: antagonist neu-
romuscular proprioceptive facilitation; AS: antagonist stretching; APS: antagonist paired set; *Significant difference versus TP; ¥ Significant difference versus
PNFA; # Significant difference versus AS.
Fig. 4. Normalized values for the SR exercise under the TP, PNFA, AS, and APS protocols; RMS values for biceps brachii, latissimus dorsi, pectoralis major and
triceps lateral head muscles were normalized to the MVIC; TP: traditional protocol; PNFA: antagonist neuromuscular proprioceptive facilitation; AS: antagonist
stretching; APS: antagonist paired set; MVIC: maximal voluntary isometric contraction; *Significant difference versus TP; ¥ Significant difference versus PNFA.
110
Paz G.A., Willardson J.M., Simão R., Miranda H. / Medicina Sportiva 17 (3): 106-112, 2013
for APS when compared to TP (P = 0.001) and PNFA
(P = 0.003) protocols; significantly greater activation
was also observed for AS versus TP (P = 0.001) and
PNFA (P = 0.002). However, no significant differ-
ences in PM and TL activation were noted between
all protocols (Fig. 4).
Discussion
The current study is the first to our knowledge, to
examine multiple antagonist pre-activation protocols
through two resistance exercises and the application of
different stretching techniques. The key finding from
the current study was the significant increase in the
number of SR exercise repetitions completed for the
APS protocol versus all other protocols; and also the
AS protocol versus the TP and PNFA protocols. The
increase in repetition performance for the APS and
AS protocols was consistent with previous studies that
involved manipulation of the antagonist musculature
as apre-activation stimulus to facilitate greater per-
formance in the agonist musculature [8,10,12,15,25].
Perhaps surprisingly, no significant increase in rep-
etition performance was evident for the SR exercise
following the contract-relax PNFA protocol versus
the TP protocol. The muscle activation data from the
current study indicated asignificant augmentation
in agonist activation (BB and LD) following the APS
and AS protocols versus the TP and PNFA protocols,
respectively. However no significant differences in an-
tagonist activation (PM and TL) was evident between
all protocols.
During the APS protocol, we noted asignificant
increase in SR repetitions versus all other protocols.
These results contrasted with those reported by Rob-
bins et al. [17] in which no differences in repetition
performance (with 4RM loads) were noted between
an APS protocol (bench pull and bench press) versus
TP (three straight sets of bench pull followed by three
straight sets of bench press) adopting 2-minute rest
interval between exercises in the APS protocol. In the
current study, asignificant increase in agonist activa-
tion (LD and BB) was observed in the APS protocol
versus the TP and PNFA protocols. However, Robbins
et al. [17] found no significant differences in the EMG
activity of the PM, LD, trapezius and anterior deltoid
when comparing the APS protocol versus the TP. How-
ever, alighter load with greater repetitions (10RM)
was instituted in the current study; and without arest
interval between the BP and SR exercises. This APS
protocol in the current study may have induced greater
fatigue in the antagonist muscles (PM and TL), which
probably contributed to the significantly greater SR
repetitions and agonist activation (LL and BB).
Asignificant increase in SR repetition performance
was also noted for the AS protocol versus the TP and
PNFA protocols. Additionally, LD and BB activation
were significantly higher during the AS protocol ver-
sus the TP and PNFA protocols. Recently, Sandberg
et al. [7] reported significantly greater isokinetic knee
extensor torque and vertical jump performance follow-
ing static stretching for the antagonist musculature;
the hamstrings were stretched prior to the isokinetic
knee extensor test and the hip flexors (single-joint)
and dorsi-flexors were stretched prior to the vertical
jump test. These authors theorized, that static stretch-
ing disrupted the length-tension relationship of the
hamstrings, leading to areduction in braking forces
which allowed an improvement on quadriceps torque
production [7]. Sharman, Cresswell and Riek [26]
stated that during adynamic muscle action, the agonist
is neurally inhibited by its own Golgi tendon organs
and by the muscle spindles of its stretched antagonist.
In the current study, the AS protocol may have elicited
asimilar disruption in the length-tension relationship
of the PM muscle, and facilitated significantly greater
SR repetitions.
Surprisingly, the PNFA protocol did not facilitate
significantly greater SR repetitions like the AS and
APS protocols. Since the PNFA protocol included 40
seconds, equally divided between contract and relax
phases; the 20 second duration of the relax phase may
have been insufficient to disrupt the braking effect of
the PM muscles as did the AS protocol which involved
40 seconds of progressive static stretching of the PM. It
was previously acknowledged that during the stretch-
ing protocols (AS and PNFA), no stretching exercises
were applied to the TL muscles because the PM is the
primary antagonist during the SR exercise. When con-
sidering the potential confounding effects of different
orders and durations of stretching multiple antago-
nists (PM and TL) it was decided to test the effects of
stretching the PM. According to Sharman et al. [26],
PNF stretching may elicit autogenic inhibition and
areduction in excitability of contracting or stretched
muscles. Franco et al. [20] reported areduction in
muscle endurance (maximum repetitions performed
at 85% of 1-RM) during aBP exercise following alow
dose of PNF stretching (one set of 20 seconds), con-
sisting of asingle stretch for the PM.
Although, in the current study the PNF stretch vol-
ume was not sufficient to significantly increase repeti-
tion performance in the agonists during the SR exercise
and concomitantly induce areduction on antagonist
activation (PM). In contrast to the current study, Paz
et al. [8] found ahigher number of repetitions com-
pleted in SR exercise (with 10RM loads) following 40
seconds of PNF stretching for the PM muscles when
compared to aSR set without pre-stretching exercise.
On the other hand, Paz et al. [8] adopted 6 seconds of
an isometric action followed by a4 second relaxation
phase repeated four times and totalizing 40 seconds.
This type of PNF protocol might elicit an acute im-
111
Paz G.A., Willardson J.M., Simão R., Miranda H. / Medicina Sportiva 17 (3): 106-112, 2013
provement in agonist repetition performance versus
the type of PNF protocol adopted in the current study
20 seconds of isometric action followed by 20 seconds
of relaxation).
Regardless of the antagonist pre-activation; in
the current study, no differences were observed on
PM and TL activation during all protocols. Another
possibility might be that the surface EMG was not
sufficiently sensitive to detect potential decreases in
the timing of antagonist activity that may have facili-
tated greater performance of the agonists for the APS
and AS protocols, respectively. The triphasic pattern
of muscle activity has been suggested as amecha-
nism to explain the enhanced acute performance of
the agonist musculature following pre-activation of
antagonist musculature [9]. This triphasic pattern is
characterized by an initial large burst of agonist activ-
ity, followed by ashorter “braking” burst of antagonist
activity, and finally asecond burst of agonist activity
during rapid or ballistic actions [12]. According to
Baker and Newton [25], apre-activation resistance
exercise for the antagonist musculature could shorten
the activation time of the braking burst and also may
facilitate alonger burst of agonist activation. Maso et
al. [6] found that the progressively RT increases the
activation of the primary motor cortex which is associ-
ated with adecrease in antagonist muscles activation
during motor tasks. The authors indicated that these
adaptations could be associated with aspecific encod-
ing of antagonist muscles activation through cortical
oscillations. In addition, Lévénes et al. [27] observed
that excitatory drive to the motor neuron pool of
the antagonist muscle is increased during fatigue of
the agonist muscle, and the different behavior of the
Hoffman-reflex and cervicomedullary motor evoked
potentials during the fatiguing action in the antagonist
muscle, suggests that the level of coactivation is likely
under the control of supraspinal rather than spinal
mechanisms.
The findings of the current study should be inter-
preted with caution because antagonist pre-activation
protocols were applied for only asingle set of aresis-
tance exercise (SR) for upper body muscles. Whereas,
atraditional RT session is composed of multiple sets
and exercises for different muscle groups. Therefore,
the current study contributes additional informa-
tion to prompt further study on the mechanism that
promoted greater agonist performance via antagonist
manipulation. The hypothesis that theorized the
improvement on agonist performance due to are-
duction in antagonist activation did not appear to be
akey mechanism accounting for the improvement
in repetitions performance. Other mechanical and
metabolic mechanisms such as elastic energy stor-
age, fatigue, and alterations in the acute sensitivity of
muscle specific proprioceptors (Golgi tendon organs
and muscle spindles) have been proposed by previous
researchers [3,6,7,9,16]. Short-term and longitudinal
studies are necessary to elucidate whether individuals
performing antagonist pre-activation protocols can
achieve greater gains in strength versus atraditional
training model.
Conclusions
The results of the current study suggested that
antagonist pre-activation through either resistance ex-
ercise or static stretching may increase acute repetition
maximum performance in the agonist musculature.
Exercise models performed using areciprocal antago-
nist/agonist protocol, as in the current study, may also
be less time-consuming and could be useful in clinical
practice as well as for sports performance training.
The antagonist pre-activation protocols (APS and AS)
also elicited significantly higher muscle activity for
the agonist muscles (LD and BB) versus the protocol
without antagonist manipulation (TP). Nevertheless,
there is justification for practitioners and coaches to
experiment with antagonist manipulation to improve
acute repetition performance and potentially longitu-
dinal training outcomes.
Declaration of interest
The authors report no conflicts of interest.
References
1. American College of Sports Medicine. Position stand. Quan-
tity and quality of exercise for developing and maintaining
cardiorespiratory, musculoskeletal, and neuromotor fitness in
apparently healthy adults: Guidance for prescribing exercise.
Med Sci Sports Exerc 2011; 43(7): 1334-59.
2. Simao R, de Salles BF, Figueiredo T, et al. Exercise order in
resistance training. Sports Med 2012; 42(3): 251-65. Epub
2012/02/02.
3. Tillin NA, Pain MT, Folland JP. Short-term unilateral re-
sistance training affects the agonist-antagonist but not the
force-agonist activation relationship. Muscle & Nerve 2011;
43(3): 375-84. Epub 2011/02/15.
4. Folland JP, Williams AG. The adaptations to strength training:
morphological and neurological contributions to increased
strength. Sports Med 2007; 37(2): 145-68.
5. Aagaard P, Simonsen EB, Andersen JL, et al. Antagonist
muscle coactivation during isokinetic knee extension. Scand
J Med Sci Sports 2000; 10(2): 58-67.
6. Maso FD, Longcamp M, Amarantini D. Training-related
decrease in antagonist muscles activation is associated with
increased motor cortex activation: evidence of central me-
chanisms for control of antagonist muscles. Exp Brain Res
2012; 220: 287-95.
7. Sandberg JB, Wagner DR, Willardson JM, Smith GA. Acute
effects of antagonist stretching on jump height, torque and
electromyography of agonist musculature. J Strength Cond
Res 2012; 26(5): 1249-56.
8. Paz GA, Maia MF, Lima VP, et al. Maximal exercise per-
formance and electromyography responses after antagonist
neuromuscular proprioceptive facilitation: Apilot study.
JEPonline 2012; 15(6): 60-7.
9. Robbins DW, Young WB, Behm DG, Payne WR. Agonist-
-antagonist paired set resistance training: Abrief review.
J Strength Cond Res 2010; 4(10): 2873-82.
112
Paz G.A., Willardson J.M., Simão R., Miranda H. / Medicina Sportiva 17 (3): 106-112, 2013
Authors’ contribution
A – Study Design
B – Data Collection
C – Statistical Analysis
D – Data Interpretation
E – Manuscript Preparation
F – Literature Search
G – Funds Collection
10. Burke DG, Pelham TW, Holt LE. The influence of varied
resistance and speed of concentric antagonistic contractions
on subsequent concentric agonistic efforts J Strength Cond
Res 1999; 13(3): 193–7.
11. Maynard J, Ebben W. The Effects of antagonist prefatigue on
agonist torque and electromyography. J Strength Cond Res
2003; 17(3): 469–74.
12. Balsamo S, Tibana RA, Nascimento DA, et al. Exercise order
affects the total training volume and the ratings of perceived
exertion in response to asuper-set resistance training session.
Int J Gen Med 2012; 5(1): 123–7.
13. Jeon HS, Trimble MH, Brunt D, Robinson ME. Facilitation
of quadriceps activation following aconcentrically controlled
knee flexion movement: the influence of transition rate. J
Orthopae and Sports Phys Ther 2001; 31(3): 122-9.
14. Robbins DW, Young WB, Behm DG. The effect of an upper-
-body agonist-antagonist resistance training protocol on
volume load and efficiency. J Strength Cond Res 2010; 24(10):
2632-40.
15. Carregaro RL, Gentil P, Brown LE, et al. Effects of antagonist
pre-load on knee extensor isokinetic muscle performance. J
Sports Sci 2011; 29(3): 271-8.
16. McBride JM, Deane R, Nimphius N. Effect of stretching on
agonist–antagonist muscle activity and muscle force output
during single and multiple joint isometric contractions. Scand
J Med Sci Sports 2007; 17(1): 54–60.
17. Robbins DW, Young WB, Behm DG, et al. Physical perfor-
mance and electromyographic responses to an acute bout
of paired set strength training versus traditional strength
training. J Strength Cond Res 2010; 24(5): 1237-45.
18. Kalmar JM, Cafarelli E. Central excitability does not limit
post fatigue voluntary activation of quadriceps femoris. J Appl
Physiol 2006; 100(1): 1757-64.
19. Soylu RA, Irmak R, Baltaci G. Acute effects of kinesiolota-
ping on muscular endurance and fatigue by using surface
electromyography signals of masseter muscle. Med Spor t
2011; 15(1): 13-6.
20. Franco BL, Signorelli GR, Trajano GS, Oliveira CG. Acute ef-
fects of different stretching exercises on muscular endurance.
J Strength Cond Res 2008; 22(6): 1832-37
21. Merletti R. Standards for Reporting EMG Data. International
Society of Electrophysiology and Kinesiology 1999.
22. Cram JR, Kasman GS. Introduction to Surfac electromyogra-
phy. ASPEM: Gaithersburg, 1998.
23. Kendall FP, McCreary EK, Provance PG, et al. Muscles, Test ing
and Function With Posture and Pain. 5 ed. Baltimore: Williams
& Wilkins, 2005.
24. Pinto RS, Cadore EL, Correa CS, et al. Relationship between
worload and neuromuscular activity in the bench press exer-
cise. Med Sport 2013; 17(1): 1-6.
25. Baker D, Newton RU. Acute effect on power output of al-
ternating an agonist and antagonist muscle exercise during
complex training. J Strength Cond Res 2005; 19 (1 ): 202-5.
26. Sharman MJ, Cresswell AG, Riek S. Proprioceptive neuromu-
scular facilitation stretching. Sport Med 2006; 36(1): 929–39.
27. Levenez M, Garland SJ, Klass M, Duchateau J. Cortical and
spinal modulation of antagonist coactivation during asub-
maximal fatiguing contraction in humans. J Neurophysiol
2008; 99(2): 554-63.
Accepted: September 4, 2013
Published: September 27, 2013
Address for correspondence:
Humberto Miranda
School of Physical Education and Sports
- Federal University of Rio de Janeiro
Av. Carlos Chagas Filho,
540. Cidade Universitária - RJ - CEP 21941-599
Tel: 55 - 21 - 2562-6808
email: humbertomirandaufrj@gmail.com
Humberto Miranda: humbertomirandaufrj@gmail.com.br
Roberto Simão: rsimaoj@terra.com.br
Jeffrey Willardson: jmwillardson@eiu.edu