An agonist-antagonist paired set (APS) refers to the coupling of exercises targeting muscle groups in an agonist-antagonist relationship, performed coincidentally in an alternating manner. For the purposes of this review, APS training will involve combinations of heavy resistance or ballistic exercises, or a combination of both, in an agonist-antagonist relationship. This review will briefly discuss the proposed benefits of APS training, the suggested underlying mechanisms, and possible implications with respect to APS training in terms of both acute performance enhancement and the development of strength and power. Furthermore, the practical applicability of APS training will be critically discussed to raise interest in determining how best to exploit it. Directions for future research will also be suggested. Finally, a common terminology (i.e., paired set) will be proposed.
Terminology: why paired set?
Somewhat confusingly, under designations such as “complex training,” “compound training,” and “supersets,” APS training has been prescribed by practitioners as a means of developing strength and power. The term “superset” is arguably the most common designation used by practitioners to describe APS training. “Superset” has been used to describe varying protocols (1,28). Generally, the term would appear to be used to describe groups of exercises (i.e., usually 2) performed successively targeting different muscle groups but can be used to describe protocols grouping exercises targeting the same muscle group. Because of the somewhat unclear definition of “superset,” and the inappropriateness of other existing terms, a more definitive term is needed (Table 1). Hence, APS is introduced as a definition limited to agonist-antagonist pairs as compared to the more broad interpretations of terms such as supersets, compound training, and others.
Empirical research has referred to APS-type training as complex (2,22,23), superset (14), and paired set training (21,24). To date, the most commonly used term in the scientific literature is complex training. A relatively large body of literature exists pertaining to complex training. However, complex training involves the coupling of biomechanically similar exercises performed in an alternating manner and is based upon the premise of performance enhancement via postactivation potentiation (19). Postactivation potentiation refers to the phenomenon by which acute muscle force output and rate of force development are enhanced as a result of contractile history. A number of varying complex training schemes have been investigated (9,20,31) and regardless of muscle group investigated, type of contraction, loading scheme, or time line between exercises, the investigations into complex training and postactivation potentiation have involved biomechanically similar exercises. Furthermore, investigations into complex training and post-activation potentiation have focused solely on augmentation of power output (PO) in the second half of the complex pair, or on chronic power development in the musculature targeted in the second half of the complex pair. More recently, 3 investigations (2,22,23) coupling biomechanically dissimilar (i.e., agonist-antagonist relationship) exercises have, perhaps erroneously, referred to this scheme as a variation of complex training. A training modality coupling biomechanically dissimilar exercises, attempting to capitalize on mechanisms other than postactivation potentiation, with intentions other than solely enhancing acute or chronic PO, should perhaps not be referred to as complex training (Figure 1). That is, APS should perhaps not be associated with terms such as complex training or postactivation potentiation. Although researchers and authors are correctly inclined to relate current research to past, to continue describing APS training as a form of complex training is arguably erroneous. A quick search in a single database (Medline) for articles with either complex training or postactivation potentiation as a key word produced over 250,000 hits. However, as previously mentioned, APS is not strictly another form of complex training with a major purpose of eliciting postactivation potentiation effects. One of the purposes of this review is to suggest a new, more appropriate term and to create interest in researching this modality. To the best of the knowledge of this group of authors, only 5 scientific investigations into APS training currently exist.
Although it may be suggested that another designation to describe training modalities in which agonist and antagonist exercises are performed in an alternating manner will further confuse, the authors argue that a common more tightly defined terminology is necessary. Agonist-antagonist paired set training would seem to be an accurately descriptive term to refer to this type of training. It is proposed that both scientists and practitioners adopt this term.
Proposed Benefits of Paired Sets
Agonist-antagonist paired set training modalities have been suggested as a means to enhance PO in an acute setting (2) and as an efficacious and time-efficient means of developing strength and power (21-24). The following is a brief discussion on each of these proposed advantages of APS training.
Acute Enhancement of Power Output
The execution of antagonist work before the performance of a ballistic activity has been suggested to enhance PO of that activity (2). However, the findings of Baker and Newton (2) are contradicted by research observing no augmentation (23), or attenuation (14), in PO after antagonist loading. The 3 studies investigating the potential for acute enhancement of PO in an APS setting implemented very different designs which may explain the varying results.
In a population of trained male athletes (i.e., 24 rugby league players), Baker and Newton (2) observed an augmentation in PO in the bench press throw 3 minutes after a set of ballistic bench pulls, compared to PO in a set of bench press throws with no intervention. It was suggested that antagonist preloading may have altered (i.e., reduced the braking period) the triphasic firing pattern during the agonist power exercise. The researchers did not incorporate a mechanistic evaluation (e.g., electromyography) into the research to support the hypothesis that antagonist preloading altered the triphasic pattern during bench press throw. Furthermore, the prescribed warm-up may have been inadequate, and therefore, any perceived augmentation in performance was possibly because of a warm-up effect. That is, the pretest or baseline set of bench press throws may have been performed in a state of incomplete warm-up and thus acted to further prepare the musculature for upcoming work. Perhaps, rather than the augmentation in performance being a result of an alteration in the triphasic pattern resulting from the antagonistic work, as suggested by the investigators, the augmentation was simply (or partially) because of a warm-up effect. It also appears that the time lines were different for the control and experimental groups. A longer rest interval between sets of bench press throw was employed by the experimental group as compared to the control group and may have influenced the results.
Robbins et al. (23) observed nonsignificant changes in power measures over 3 APSs, in which bench press throws were preceded by bench pulls in a population of trained, university-aged male athletes. Their research also reported nonsignificant differences in electromygraphic (EMG) activity in the APS as compared to a “traditional” protocol, in which all sets of the first exercise (bench pull) were performed before all sets of the second exercise (bench press throw). A nonballistic intervention would not be expected to affect the triphasic pattern. The lack of augmentation in bench press throw performance reported in the study by Robbins et al. (23) may have been because of the implementation of a nonballistic intervention (4 repetition maximum [4RM] bench pull) performed with low repetitions (with a tendency to decrease from sets 1 to 3), as compared to the intervention used by Baker and Newton (2) of 8 ballistic bench pulls. It is also possible, although perhaps unlikely, that performance was enhanced to a similar extent in all 3 sets of APS bench press throw. This would not have been observed as a set of bench press throw without intervention (e.g., before the first set of bench pull) was not performed. However, the 3 sets of bench press throw performed under the APS condition were not only similar to one another but also similar to the 3 sets of bench press throw performed under the “traditional” condition. That is, if some augmentation occurred repeatedly and to the same extent over 3 sets under the APS condition, it must also have occurred under the “traditional” condition. It would seem unlikely that a similar level of augmentation occurred in each set of bench press throw, under both conditions, as a result of the cumulative effects of the varying exercise performed before that set. Rather, it would seem more likely that there was no augmentation in performance.
Maynard and Ebben (14) also failed to observe enhancement in performance in a population of trained, male collegiate athletes completing maximal isokinetic knee flexion and extension exercises. These researchers found a decrease in peak torque, rate to peak torque, and peak power production in the agonist musculature when the antagonist muscle group was prefatigued. They measured the EMG activity of the agonist and antagonist musculatures and suggested that perhaps the observed increase in EMG activity of the antagonist (co-contraction) may have been responsible for the attenuation in performance measures. It should be noted that the investigators implemented a warm-up that included static stretching. It is generally accepted that static stretching is not advised before performance (6,30). One could argue that, similar to the Baker and Newton (2) study, the warm-up was inadequate, and this may have confounded the results. It is unclear if there is a differential response in the upper body as compared with the lower body. A greater level of coactivation in the antagonist musculature may manifest itself as fatigue and affect that muscle group adversely when acting as an agonist.
Of the 3 studies to date (2,14,23) that have attempted to enhance PO after loading of the antagonist musculature, only Baker and Newton (2) reported augmentation. The study by Baker and Newton (2) was the only one in which a ballistic intervention was used in the upper body. If the intent of a training protocol is to enhance acute PO via an antagonist intervention, it would seem likely that the nature of the intervention is important. It may be that in accordance with the principle of specificity, upper body ballistic movements can be augmented via an antagonistic ballistic movement. However, because of the limited and equivocal nature of the evidence, any conclusions would seem premature.
Strength and Power Development
It has been suggested that APS training is an efficacious means of developing strength and power (22). Over the course of an 8-week training period, a group of trained, male collegiate athletes performing APS training were reported to achieve similar increases in 5 performance measures (1RM bench pull and bench press, throw height, peak velocity, and peak power) as compared with the increases achieved by a similar group which performed a “traditional” protocol in which all sets of pulling exercises were performed before pushing exercises in all training sessions (22). Under the APS condition, 1RM bench pull and bench press increases were statistically significant, whereas the increases observed in the monitored power measures were not, leading the researchers to hypothesize that APS modalities may be better suited to strength, as compared to power, development. Although the increases in the monitored power measures were not statistically significant under the APS condition, the increases were similar to those observed under the “traditional” condition. At this time, there is no reason to believe that APS training holds any advantages over traditional training schemes with respect to the development of power.
The obvious dearth in research makes any recommendations difficult at this time. With respect to the only longitudinal study to date (22), it should be noted that the sample sizes were relatively small (i.e., 7 in the traditional group and 8 in the APS group), and therefore, the power to detect statistically significance differences in the dependent measures under one, or both, of the conditions may have been limited. Furthermore, it is possible that the relatively low prescribed training volume (i.e., 18-25 repetitions per muscle group, per session) and frequency (2 sessions per week) did not provide a great enough stimulus over the 8-week period to produce significant results in all measures, under both conditions, in the relatively highly trained participants (i.e., minimum one- and generally several-years experience). Perhaps longer (i.e., more repetitions) or more frequent (i.e., more than 2 times per week) training sessions over the course of the 8 weeks would result in statistically significant gains being evident. However, it is important to note that regardless of the relatively small sample sizes, low volume, and infrequency, statistically significant increases in both strength measures were observed under the APS condition, making a strong case for the efficacy of APS strength training. Although the lack of research makes recommendations difficult, it does appear that APS training may hold some merit as a means of developing strength.
Possibly the most intriguing role of APS training may be as a time-efficient method of developing strength and power. It has been hypothesized that in the event of similar, or even compromised (i.e., lesser), outcomes under APS as compared to other more time-consuming modalities (e.g., modalities not targeting the antagonist musculature during rest intervals between agonist work), APS training may be considered a time-efficient modality (21-24). Acute (output·time−1, where output is the dependent measure, and time refers to the time taken to achieve that output) and chronic (effect·time−1, where effect is the dependent measure and time refers to the time taken to achieve that effect) efficiency calculations were performed in 4 studies (21-24) and determined APS training to have enhanced efficiency as compared with “traditional” conditions in which agonist musculature was targeted before antagonist musculature. Enhanced efficiency was observed with respect to all but one of the performance measures in one of the studies. Furthermore, effect size statistics performed in all 4 studies supported the determination that APS training enjoyed enhanced efficiency. Specifically, large effect sizes were observed in 10 of the 13 performance measures.
Three of the 4 studies that performed efficiency calculations were acute in nature. As previously discussed, Robbins et al. (30) investigated an APS coupling of bench pull and bench press throw performed over 3 sets and compared the outcomes to a “traditional” protocol and determined that although bench pull volume load (load × repetitions) decreased over the 3 sets, it did so to a similar extent under both conditions. Bench press throw performance was maintained over the 3 sets, and was similar under both conditions. Similar maintenance of throw height, peak velocity, and peak power in the bench press throw exercise, volume load in the bench pull and similar EMG signal under APS as compared with the “traditional” condition indicate similar stress was imposed on the musculature in approximately half the time, suggesting efficiency is enhanced under APS training. Efficiency calculations and effect sizes from that study are presented in Table 2. In a subsequent study, Robbins et al. (24) investigated an APS coupling of 2 heavy resistance training exercises (bench pull and bench press) performed over 3 consecutive sets, and reported that although volume load decreased from set 1 to set 2 and from set 2 to set 3, there were no differences in volume load over the 3 sets, or over the sessions, in APS as compared to a “traditional” condition. Because similar volume loads were achieved under the less time-consuming APS condition, it was concluded that APS training was more efficient. Efficiency calculations and effect sizes from that study are presented in Table 2. Although there was a significant within-set EMG activity response in the bench press exercise, EMG activity was not different under the 2 conditions, suggesting that the level of neuromuscular fatigue did not differ under APS as compared to the “traditional” condition. A subsequent investigation involving similar exercises (i.e., bench pull and bench press) compared an APS to a “traditional” condition but did so in a manner in which the time to complete the sessions was constant (21). That is, the denominator (time) in the efficiency calculation (output·time−1) was similar under both conditions. Over 3 sets, bench pull and bench press volume load decreased significantly from set 1 to set 2 and from set 2 to set 3 under both the APS and traditional conditions. Bench pull and bench press volume load per set were significantly less under the traditional as compared to APS condition over all sets, with the exception of the first set (bench pull set 1) in the sessions. Efficiency calculations and effect sizes (large) from that study are presented in Table 2 and indicate APS training, as compared to the “traditional” condition, enjoyed enhanced efficiency under circumstances in which time lines were similar. These studies only examined APS training performed over 3 sets. It is possible that over longer training sessions, different outcomes could result in conclusions deeming APS inefficient (output·time−1). However, with respect to the 2 acute studies with varying time lines (i.e., APS completed in half the time required to complete the traditional protocol), volume load would have to be compromised by more than 50% to deem APS training inefficient. Such an outcome is perhaps unlikely. With respect to the study in which time lines were similar, there is no reason to believe (i.e., lack of supporting evidence) a reversal in the observed trends whereby volumes loads were significantly less under the “traditional” as compared to the APS condition over all sets, would occur.
Under a previous section, “Strength and Power Development,” the results from a longitudinal study (22) were presented. Because the increases in performance measures were similar under both conditions, the reduced time necessary to complete the APS sessions suggested that APS training is time efficient with respect to the development of 1RM bench pull and bench press, peak velocity and peak power. Efficiency calculations and effect sizes from that study are presented in Table 2. Although limited, research into APS training that has calculated efficiency is unequivocal in the determination that APS training is a time-efficient training modality. Agonist-antagonist paired set training can be recommended to those desiring to complete training sessions in less time, yet still achieve similar results as traditional training.
The mechanisms underlying APS training are not well investigated and are unclear. To more completely exploit APS training, it is necessary to better understand the underlying mechanisms. Mechanisms that have been suggested to influence APS-type training include alteration in the triphasic firing pattern (2) and phenomena associated with fatigue, such as increased motor unit activation and increased activation of synergist and antagonist muscles (22-24). Although mechanisms associated with phenomena such as the stretch shortening cycle have been suggested to be implicated in agonist-antagonist movement pairs, the authors would argue that the nature of APS training (i.e., the time between antagonist and agonist exercises and the independent character of the 2 exercises) precludes the involvement of such mechanisms. The time between agonist and antagonist contractions necessary to elicit responses associated with stretch shortening cycle movements is less than 1 second (11). Rather, the mechanisms are likely linked to coactivation (2) and contractile history (22-24). The contractile response of skeletal muscle is partially determined by its contractile history (13). With respect to APS training, the contractile history of both the agonist and antagonist musculature must be considered.
Muscular fatigue can refer to a decrease in force-generating capacity (3,4). A number of mechanisms, including neuromuscular and metabolic, are responsible for the decrease in force-generating capacity. Metabolic fatigue at the cellular level can be attributed, at least in part, to the accumulation of a number of metabolic byproducts, all or some of which may disturb actomyosin cycling, Ca2+ sequestration and Na+/K+ exchange, thereby resulting in fatigue (8,16). Nonmetabolic fatigue can also result from intense activity and is characterized by myofibrillar disorientation and cytoskeletal damage (8).
Agonist-antagonist paired set training is arguably more fatiguing than training modalities in which antagonist work is not performed during the rest intervals between agonist exercise sets. Although the rest interval between like exercises is similar in APS- and “traditional”-type protocols, the training density (work·time-1) is greater under APS, and extended bouts (i.e., more than 3 sets) of APS training are likely more fatiguing. If, extended bouts of APS training are indeed more fatiguing than “traditional” training modalities, this may help to explain the chronic outcomes reported by Robbins et al. (22) and subsequent suggestions. Specifically, the suggestion that APS-type protocols may be better suited to developing strength as compared to power, and that the reverse is true with respect to “traditional-type” protocols. It was hypothesized that the level of fatigue (i.e., greater fatigue under APS because of less total rest time during training sessions) may have played a role in the outcomes (22). Greater levels of fatigue in subsequent power training sets would negatively impact movement velocity directly inhibiting a key factor in power development. It is possible that elevated levels of fatigue, as a result of the increased training density inherent in APS training, may facilitate strength development over extended training periods.
Fatigue may act as a stimulus, which leads to increases in strength (25). These researchers maintained a constant volume load and varied rest intervals between contractions. They determined that no rest between contractions led to greater strength gains than resting between contractions. It is possible to infer from these findings that in the event volume load is compromised (using similar rest intervals) under APS- as compared to “traditional”-type conditions, this may not adversely affect chronic gains in strength. In fact, it is possible that a reduced volume load as a result of fatigue may lead to greater gains in strength over a prolonged training period. The principle of specificity suggests this factor (i.e., fatigue acting as a stimulus) may be less likely with respect to power development. It is generally accepted that repeatedly achieving greater POs in an acute setting over a prolonged period will lead to greater chronic adaptation, as compared with prolonged training at a lower level (29). That is, with respect to power, training at a higher level will result in adaptation at a higher level. Thus, the argument that fatigue may be beneficial to strength and detrimental to power development may perhaps explain the chronic outcomes reported by Robbins et al. (22).
The neuromuscular mechanisms by which fatiguing contractions may lead to increases in strength are unclear. It has been suggested that training protocols which produce fatigue result in greater motor unit activation than nonfatiguing protocols and that the level of motor unit activation determines the size of the training response (25). Alternatively, it has been suggested that fatigue might provide a more appropriate setting in which to encourage activation of synergist and antagonist muscles and thereby increase the training response, or that some relationship might exist between events related to fatigue and events that trigger muscle adaptation (25). Robbins et al. (22) reported no changes in EMG activity pre to posttraining under either the APS or “traditional” condition. It is therefore difficult to postulate as to the appropriateness of the above suggested mechanisms, by which fatigue may act as a stimulus for strength, with respect to that study. Furthermore, Robbins et al. (22) did not monitor EMG signal during training sessions under either condition. It is therefore difficult to comment on the level of fatigue resulting from APS as compared with “traditional” training sessions in which greater than 3 sets are completed.
Coactivation refers to the concurrent activation of agonist and antagonist muscles (7,18). The antagonist musculature slows the movement initiated by the agonist musculature in such a way as to allow for controlled movement. It has been suggested that this concurrent activation may increase joint stability, aid in the prevention of injury and help to control limb position (4,5,10,11,26). Thus, coactivation may work to improve (e.g., through movement control) or inhibit (e.g., through stiffening) performance.
Augmentation of subsequent agonist contractions might be attributed to a number of possible antagonist contraction-related mechanisms. These mechanisms might include (a) alterations to the triphasic pattern of ballistic contractions; (b) antagonist prefatigue decreasing resistance to the intended movement; and (c) enhanced activation of agonist because of reciprocal innervation. The following paragraphs will attempt to discuss each of these possible mechanisms in relation to the current APS literature.
Alteration of the triphasic coactivation pattern (i.e., shortening of the antagonist braking period) as a result of antagonist preloading has been suggested as a possible mechanism responsible for performance enhancement (2). Research into APS training as a means of enhancing acute performance has focused on movements involving high rates of power development (2,23). These movements are commonly performed in an explosive or ballistic manner. Ballistic movements have been associated with a triphasic pattern whereby there is an initial burst from the agonist musculature, followed by a burst from the antagonist musculature, and then a final burst from the agonist musculature (32). Arguably, a shortening of the antagonist braking burst would allow for a larger aggregate agonist firing period and could conceivably result in performance enhancement. Unfortunately, the researchers (2) who put forward this theory did not incorporate the measurement of EMG activity data into the research design to support this postulation. Therefore, any suggestion that PO may be augmented via the alteration of the triphasic pattern as a result of antagonist preloading is speculative at this time.
Prefatiguing the antagonist may decrease the resistance to the intended movement resulting in enhanced performance of agonist force output. It is possible that this, rather than alteration of the triphasic pattern, may have been responsible for the enhancement in PO observed by Baker and Newton (2). One might wonder why a similar augmentation was not observed by Robbins et al. (23) or Maynard and Ebben (14) as the antagonist musculature was prefatigued under the protocols implemented by both groups of researchers. Perhaps the time line of any decrease in resistance resulting from prefatiguing of the antagonist was not captured because of an inappropriate rest interval between antagonist and agonist activity. Alternatively, the load or type of contraction may have been inappropriate or at least was inappropriate in conjunction with the rest interval. It is also possible that factors such as training status, training age, chronological age, genetics (i.e., fiber-type composition), anthropometry, relative strength, or absolute strength may have played a role.
Enhanced activation of the agonist musculature because of reciprocal innervation (12,15,17) could result in augmentation of PO. Again, it is possible that this mechanism, rather than alteration of the triphasic pattern, may have been responsible for the enhancement in PO reported by Baker and Newton (2). Perhaps if a submaximal intensity bout of antagonist contractions was used by Robbins et al. (23) or Maynard and Ebben (19), then a reciprocal innervation-induced activation of agonists would prevail over lingering fatigue affects.
Although the above-discussed mechanisms associated with coactivation are generally accepted, evidence that these phenomena can be manipulated through APS training to result in performance enhancement does not exist. At this time, any suggestions as to how coactivation and associated mechanisms can be exploited via APS training are speculative. Research incorporating mechanistic approaches (e.g., EMG) is necessary to draw conclusions as to the role of coactivation in APS training.
Exploitation Of Paired Sets
It has been hypothesized that APS training may be exploited to achieve short-term enhancement of PO (2) and to achieve chronic adaptation through training and thereby improve performance (23). Factors deserving of consideration before attempting to capitalize on APS training in an acute or chronic setting will be presented in this section.
Acute Enhancement of Performance
Before any attempt to enhance acute athletic performance through the manipulation of antagonist contractile history via APS training, a number of variables need to be considered. The training variables requiring consideration include type of contraction (i.e., isometric, concentric-eccentric, multijoint, etc.), intensity, volume (i.e., repetitions, sets, cadence, time under tension), rest interval(s) between possible multiple sets, rest interval within the APS couple, and responses of varying muscle groups. It is also possible that, as with many training modalities, interindividual variability could further confound any attempt to manipulate antagonist contractile history for the purpose of enhancing performance. Because interindividual variability exists, a number of categorical variables would also need to be considered. These include training status, training age, chronological age, genetics (i.e., fiber-type composition), anthropometry, gender, relative strength, and absolute strength. Before any conclusions can be made as to the efficacy of APS training in a warm-up protocol designed to enhance performance, further scientific research is necessary.
Strength and Power Development
Before designing APS training schemes aimed at developing strength and power, many of the same variables (training and categorical) considered with respect to acute performance enhancement would need to be taken into account. Depending on the combination of exercises, an APS protocol may be intended to develop strength or power or hypertrophy or any combination of these (Figure 1). Training variables will tend to differ depending on the type (i.e., strength or power or hypertrophy or combination) of APS protocol and the goal(s) of that protocol.
Based on the above discussion, some recommendations can be made regarding APS training with respect to acute performance enhancement, chronic development of strength and power and time efficiency. With respect to acute performance enhancement, 2 discussions are warranted. Firstly, a discussion as to the practical applicability of APS training as a means to enhance performance precompetition, and secondly as a means by which to train at a higher level and thereby adapt at a higher level.
As a means to enhance competitive performance in an acute setting, APS may be of questionable benefit. The evidence suggesting that antagonist preloading results in enhancement of power focused performance is limited and equivocal. If antagonist contractile history can be manipulated to result in acute enhanced performance, the question of feasibility is raised. It would be a considerable task to determine training variable parameters for countless different athletic profiles. Assuming training variables were determined in conjunction with categorical variables, a myriad of other implications could For example, possible practicality problems could include (a) the availability of equipment at the site of competition; (b) coordinating the potentiation and fatigue time lines within the competition time line; and (c) cumulative effects over the course of repeated trials (e.g., high jump).
Issues of transferability could also arise. Whereas a certain stimulus may act to enhance performance of a given activity, it may not act to enhance performance of a different activity. Experiments would be necessary to determine the applicability of APS to various athletic activities. Furthermore, any suggestion that antagonist preloading be employed before competition with the intention of enhancing competitive performance would seem problematic without first determining a number of training variables appropriate to that competitor or group of homogeneous competitors. Given the issues of practicality and equivocal nature of evidence to date, it would seem problematic to prescribe an APS-type warm-up protocol before competition without further research confirming the effectiveness of such a modality.
Theoretically, if PO could be consistently augmented in an acute training setting, enhanced adaptation may occur. As a means to develop power in a gym setting, issues with practicality are less pronounced. Presumably, equipment is available and time lines can be controlled. However, even if APS training is feasible in a training setting, evidence indicating it is advantageous in terms of acutely enhancing PO remains limited and equivocal. Any suggestion that antagonist preloading results in power performance enhancement is premature.
Although limited, evidence exists suggesting APS training is an efficacious means of developing strength and power. The suggestion by Robbins et al. (22) that APS training may be better suited to strength, as compared to power adaptation, is interesting and deserves further attention. Practitioners working with athletes or the general population may be well advised to consider APS training as a means of developing strength. With respect to the development of power, practitioners may wish to be more cautious. Although Robbins et al. (22) reported similar increases in power measures under the APS, as compared to the “traditional” condition, the presented effect size statistics (Table 1) suggest that perhaps APS training is not particularly well suited to power adaptation. Although APS training would appear to be an effective method of developing strength, recommendations with respect to power adaptation may be ill-advised at this time. Before the completion of further research, APS pairings designed to develop strength (e.g., combinations of heavy exercises) may be more appropriate than pairings aimed at developing power (e.g., incorporating ballistic exercises).
Perhaps the most confident recommendation can be made with respect to APS training as an efficient training modality. The results of research to date (see Table 1) overwhelmingly suggest that APS training is a time-efficient method by which to develop strength and power. In the absence of significant differences (acute or chronic) between traditional modalities and APS training, it could be argued that APS training elicits results similar to those of more traditional training methods but in a more time-efficient manner. Resistance training modalities that aim to enhance musculoskeletal conditioning have been associated with improved health and a decrease in the risk of chronic disease and disability (27). Athletes and trainers face a number of challenges in preparation for competition, and the general population faces challenges with respect to the maintenance of health and wellness. Time is a constraint, and one such challenge, for athletes and the general population. Efficient resistance training schemes that do not compromise efficacy, or increase efficiency, could be advantageous to not only athletes but also the general population.
Attempts have been made to examine the practical applicability of APS with respect to enhancing acute athletic performance, the efficacy of APS training as a means to develop strength and power, and as a time-efficient training modality. The results discussed in the literature regarding the enhancement of acute performance are equivocal, and the task of determining possible parameters allowing for consistent enhancement of acute performance is a daunting one. With respect to chronic adaptation, some evidence does exist to suggest that APS training is at least as beneficial, and more time efficient, as other comparable training methods designed to develop strength and power (22). At present, the existing body of literature would seem to suggest that the practical applicability of APS with respect to enhancing acute athletic performance is limited. Agonist-antagonist paired set training may be an efficacious and efficient method of developing strength and, to a lesser extent, power.
Practitioners and researchers need to be aware that the recommendations presented above follow from the limited evidence available. To better understand possible benefits of APS training and the associated underlying mechanisms, further research is necessary. There are many questions that remain unanswered, and researchers are encouraged to take a mechanistic research approach to further elucidate the potential benefits of APS training. Areas deserving of future research include (a) acute power augmentation in the upper and lower body; (b) strength and power development in the upper and lower body; and (c) APS training aimed at hypertrophy.
Within these areas are a multitude of unanswered questions related to the appropriate type of contraction, intensity, volume, rest intervals between possible multiple sets, rest interval within the APS couple, and the responses of varying muscle groups. Individual- or group-specific categorical variables also deserve attention. Researchers are further encouraged to consider time efficiency regardless of the question and design. Some questions that remain unanswered include the following: (a) “Can antagonist ballistic movements enhance subsequent agonist PO in the upper body? Lower body?”; (b) “Can APS be used to develop strength in the upper body? Lower body?”; (c) “Can APS be used to develop power in the upper body? Lower body?”; and (d) “Can APS be used to develop hypertrophy in the upper body? Lower body?”. With respect to these questions, the appropriate loading scheme and rest interval between agonist and antagonist work and between sets would need to be determined, creating a number of subquestions.
1. Anning, J. A practical comparison of different lower body resistance training modes. NSCA's Performance Training Journal, 7.1. Retrieved Feb. 7, 2008, from http://www.nsca-lift.org/Perform/Issues/0701.pdf
2. Baker, D and Newton, RU. Acute effect on power output of alternating an agonist and antagonist muscle exercise during complex training
. J Strength Cond Res
19: 202-205, 2005.
3. Barnett, CH and Harding, D. The activity of antagonist muscles during voluntary movement. Ann Phy Med
2: 290-293, 1955.
4. Basmajian, JV and DeLuca, CJ. Muscle Alive. Their Functions Revealed by Electromyography
ed.). Baltimore, MD: Williams and Wilkins, 1985.
5. Behm, DG. Muscle force and activation under stable and unstable conditions. J Strength Cond Res
16: 416-422, 2002.
6. Behm, DG, Bambury, A, Cahill, F, and Power, K. Effect of acute static stretching on force, balance, reaction time, and movement time. Med Sci Sport Exer
36: 1397-1402, 2004.
7. De Luca, CJ and Mambrito, B. Voluntary control of motor units in human antagonist muscles: coactivation and reciprocal activation. J Neurophysiol
58: 525-542, 1987.
8. Green, HJ. Mechanisms of muscle fatigue in intense exercise. J Sport Sci
15: 247-256, 1997.
9. Hrysomallis, C and Kidgell, D. Effect of heavy dynamic resistive exercise on acute upper-body power. J Strength Cond Res
15: 426-430, 2001.
10. Kellis, E and Kellis, S. Effects of agonist and antagonist muscle fatigue on muscle coactivation around the knee in pubertal boys. Electromyogr Kines
11: 307-318, 2001.
11. Komi, PV. Stretch-shortening cycle: A powerful model to study normal and fatigued muscle. J Biomech
33: 1197-1206, 2000.
12. Levine, MG and Kabat, H. Cocontraction and reciprocal innervation in voluntary movement in man. Sci Wash DC
116: 115-118, 1952.
13. MacIntosh, BR and Rassier, DE. What is fatigue. Can J Appl Physiol
27: 42-55, 2002.
14. Maynard, J and Ebben, WP. The effects of antagonist prefatigue on agonist torque and electromyography. J Strength Cond Res
17: 469-474, 2003.
15. Moore, MA and Hutton, RS. Electromyographic investigation of muscle stretching techniques. Med Sci Spor Exer
12: 322-329, 1980.
16. Noakes, TD, Lambert, EV, and St Clair Gibson, A. The ATP paradox-Why muscles do not develop rigor during exercise. Med Sci Sport Exer
33: S95, 2001.
17. Patton, NJ and Motenson, OA. An electromyographical study of reciprocal activity of muscles. Anat Res,
170: 255-268, 1971.
18. Psek, JA and Cafarelli, E. Behaviour of coactive muscles during fatigue. J Appl Physiol
74: 170-175, 1993.
19. Robbins, DW. Postactivation potentiation and its practical applicability: A brief review. J Strength Cond Res
19: 453-458, 2005.
20. Robbins, DW and Docherty, D. Effect of loading on enhancement of power performance over three consecutive trials. J Strength Cond Res
19: 898-902, 2005.
21. Robbins, DW, Young, WB, and Behm, DG. The Effect of an Upper Body Agonist-antagonist Resistance Training Protocol on Volume Load and Efficiency
. J Strength Cond Res,
22. Robbins, DW, Young, WB, Behm, DG, and Payne, WR. Effects of agonist-antagonist complex resistance training on upper body strength
and power development. J Sport Sci
27: 1617-1625, 2009.
23. Robbins, DW, Young, WB, Behm, DG, and Payne, WR. The effect of a complex agonist and antagonist resistance training protocol on strength
and power output, electromyographic responses and efficiency
. J Strength Cond Res
24: 1782-1789, 2010.
24. Robbins, DW, Young, WB, Behm, DG, Payne, WR, and Klimstra, MD. Physical performance and electromyographic responses to an acute bout of paired set strength
training versus traditional strength
training. J Strength Cond Res
24: 1237-1245, 2010.
25. Rooney, KJ, Herbert, RD, and Balnave, RJ. Fatigue contributes to the strength
training stimulus. Med Sci Sport Exerc
26: 1160-1164, 1994.
26. Solomonow, MR, Baratta, R, Zhou, B, and D'Ambrosia, R. Electromyogram coactivation patterns of the elbow antagonist muscles during slow kinetic movement. Exp Neurol
100: 470-477, 1988.
27. Warburton, DE, Nicol, CW, and Bredin, SS. Prescribing Exercise as Preventative Therapy. Can Med Assoc J
174: 961-974, 2006.
28. Wathen, D. Strength
training and spotting techniques. In: Essentials of Strength Training and Conditioning
. Baechle, TR, ed. Champaign, Il: Human Kinetics, 1994. pp. 435-400.
29. Wilson, G, Newton, R, Murphy, A, and Humphries, B. The optimal training load for the development of dynamic athletic performance. Med Sci Sport Exer
23: 1279-1286, 1993.
30. Young, W, and Behm, D. Should static stretching be used during a warm up for strength
and power activities? J Strength Cond Res
4: 33-37, 2002.
31. Young, W, Jenner, A, and Griffiths, K. Acute enhancement of power performance from heavy load squats. J Strength Cond Res
12: 82-84, 1998.
32. Zehr, PE and Sale, DG. Ballistic movement: Muscle activation and neuromuscular adaptation. Can J Appl Physiol
19: 363-378, 1994.