CAN TRAINING IMPROVE YOUR ABILITY TO CO-CONTRACT? Jordan Yurchevich. St. Francis Xavier University. October 9, 2006

Transcription

1 CAN TRAINING IMPROVE YOUR ABILITY TO CO-CONTRACT? Jordan Yurchevich St. Francis Xavier University October 9,

2 Introduction The aim of the present study is to determine whether or not training can enable an individual to increase the amount of resistive force produced by an antagonistic muscle in a maximal voluntary isometric contraction. Although it may seem contradictory to contract these opposing muscle groups simultaneously, this idea of cocontraction is regularly observed within normal muscle functioning. Coactivation of agonist-antagonist muscle pairs has been demonstrated to be important in joint stability (Barratta et al., 1988; Gabriel, Basford, & An, 1997; De Luca & Mambrito, 1987) and learning new motor tasks (Calder & Gabriel, 2006). This information suggests the functional importance of being able to cocontract muscles. Much research has investigated the mechanism of muscle activation and contraction. Very simplistically, a signal sent from the central nervous system is propagated along efferent nerves towards a muscle. Once the signal reaches the muscle, a series of events are triggered in the muscle whereby calcium ions are released allowing for contraction of the muscle. Less is known in regards to the mechanism controlling the simultaneous contraction of opposing muscles. For example, in a extension movement, is it a complimentary connection in which the flexor is inhibited to allow more efficient control of the extensor, or is it an overriding process where both flexor and extensor are activated with the extensor simply having more stimulation? De Luca and Mambrito (1987) suggest that there is a common drive mechanism that controls the musculature and, depending on the action, there is a different form of control. In understanding this control, together with knowing that resistance training has been shown to result in either physiological or neurological adaptations (Sale, MacDougall, Always, & Sutton, 1987; Sale, 1988), the idea of a common drive 2

3 may possibly be used to create resistance training programs that elicit simultaneous adaptations in both agonist and antagonist. Monitoring changes in electrical activity within the muscles by means of electromyography can reveal whether or not neurological adaptation has occurred (Sale, 1988). Interpreting the electromyographic (EMG) activity allows one to make valid predictions on the maximal contractile force that is being produced by the muscle. Any neurological adaptations that may occur in response to the stresses of training will result in an increased ability to generate force within the muscle, as represented by increases in EMG activity (Moritani & de Vries, 1979). Externally inducing a contraction in an antagonistic muscle has been shown as an effective means of producing a resistive force to the agonist, as well as improving the maximal force produced by the agonist and antagonist (Yanagi et al., 2003). The current investigation will determine if it is possible to train an individual s ability to cocontract to a point where enough resistance can be created with the antagonist muscle to train its opposing agonistic muscle. Literature Review Sherrington s work on the neuromuscular system and reciprocal innervation (as cited in De Luca, & Mambrito, 1987, set the stage for numerous investigations into the mechanism behind the control of antagonistic muscles. De Luca and Mambrito (1987), for example, suggest that antagonists may be controlled by a common drive. Results from the study showed that the motor units (MU) of the agonist and antagonist fired in unison. This suggests that there is some central control over the firing rate which acts uniformly on the entire motoneuron pool innervating antagonistic muscles, rather than on individual MU. De Luca and Mambrito (1987) also propose a three-channel model for 3

4 the control of antagonistic MU. This model states that separate flex and extend commands exist to control reciprocal actions, while the third command, coactivation, controls the pure co-contraction of the antagonistic muscles. These two concepts of common drive and the three-channel model work together in muscle activity. During flexion, the flexor MU would be stimulated through the action of the common drive on the flexor motoneuron pool. This would cause excitation in the agonist while inhibiting the antagonist. The opposite would be true for extension. Coactivation, however, requires a different method of control. If the flexion and extension commands were simultaneous, then the excitation and inhibition would cancel each other out (De Luca & Mambrito, 1987). The coactivation command would therefore act on a coactivation motoneuron pool which would have an excitatory effect on both agonist and antagonist. This notion of different controls for the different aspects of agonist/antagonist contraction states is supported by electophysiological evidence provided by Frysinger et al. (1984), as well as research conducted by Nielsen and Kagamihara (1994). The thoughtful implementation of these principles into a strength training program may be able to elicit a neural adaptive response in both agonist and antagonist. In fact, there is research suggesting the level of coactivation in antagonistic muscles is trainable through some form of resistive training (Colson, Pousson, Martin, & Van Hoecko, 1999; Gabriel, Basford, & An, 1997; Carolan & Cafarelli, 1992). Resistance training typically results in physiological adaptation (Sale, 1988; Farina, Merletti, & Enoka, 2004), as well as rapid neuromuscular adaptation (Pucci, Griffin & Carafelli, 2006; Sale, 1988; Chilibeck, Calder, Sale, & Webber, 1998). These neuromuscular adaptations include, among others, changes in neuronal firing rate and 4

5 motor unit recruitment. Pucci et al. stated that dynamic resistance training increases the maximal motor unit firing rate, as opposed to isometric training, which has no effect. Sale (1988) proposed that resistance training may lead to changes within the nervous system resulting in an increased ability to activate agonistic muscles. Although resistance training is primarily focused on inducing adaptations in agonistic muscles, several researchers have examined the adaptations in the antagonist muscle in response to training. This research has provided conflicting results, as some evidence suggests decreased antagonistic neural activity (Carolan & Cafarelli, 1992), while others suggest otherwise (Colson et al., 1999). Electromyographic analysis of the muscular electrical activity can provide an indication as to whether neural adaptation has occurred in these muscles (Sale, 1988). Surface electromyography (semg) amplitude is directly related to the neural activity of the monitored muscles (Farina, Merletti, & Enoka, 2004). Gabriel (2000), and Gabriel and Boucher (1998), suggest that increases in both signal frequency and spike content of semg are indicative of muscle activity changes due to training. Similarly, it has been shown that increases in semg amplitude are a result of increased motor unit recruitment and/or firing rate (Farina et al., 2004). Differentiation between the two has been determined impossible due to several limitations as discussed by Farina et al. (2004). Moritani and de Vries (1979) demonstrated that initial strength gains, as a result of strength training, are due to neural adaptations. These strength gains will be visible as an increase in the maximal force production of the muscle, which in turn can be determined through interpretation of EMG activity in the muscle. 5

6 Recently, Yanagi et al. (2003) implemented a novel resistance training technique utilizing neuromuscular electrical stimulation (NMES) to contract an antagonistic muscle while having their subjects perform concentric contractions against that resistance. The results of this study suggested that the hybrid strength training technique was effective at producing physiological adaptations and strength gains. As semg was not incorporated into this study, there was no way of determining if any neurological adaptation took place in either agonist or antagonist. Though this training technique has obvious advantages in rehabilitation settings (Yanagai et al., 2003), if one could eliminate the NMES aspect while maintaining adequate resistance provided by the antagonistic muscle, such as through maximal voluntary contraction (MVC) of the antagonist, this beneficial training method would be accessible to a much larger population. Therefore, the purpose of this study is to determine if co-contraction resistance training can improve an individual s ability to provide resistance with their antagonist muscles. Specifically, the investigation will look at whether a 6-week training regimen whereby the contracted triceps brachii (TB) is used as resistance in the concentric, as well as eccentric, contraction of the biceps brachii (BB) can improve an individual s ability to increase the resistance provided by the TB in maximal voluntary isometric contraction (MVIC). It is expected that through training, the subjects will be able to increase the resistance provided by the TB, and in turn develop more neural activity in both the BB and TB. 6

7 Methods Subjects For the current investigation, right-handed university aged females will be recruited through the use of posters, flyers, word of mouth, and . The emphasis on females is due to the trial and day error variances of men, which have been demonstrated to be between two and four times higher than in women (Kroll, 1970). The subjects will have little or no weight training experience, and will not have trained within the previous six month. As well, weight training throughout the study will not be permitted. The exercises, risks, testing procedures, and time required will be explained to each of the participants before they read and sign the informed consent documentation. Apparatus, Testing Position, and Testing Schedule EMG data will be obtained from a pair of silver-chloride surface electrodes applied to the belly of the biceps brachii (BB), and a pair applied to the lateral head of the triceps brachii (TB). Light abrasion of the skin where the electrodes are to be placed will help to keep the impedance low at the skin-electrode interface. Center-to-center distance between electrodes will be 16mm, with the reference electrode placed on the opposite wrist. Indelible ink will be used to mark (and remark at each training session) the exact location and position of the electrodes. This will aid in keeping the electrode placement consistent throughout the duration of the study. The signals will be amplified with a bandwidth frequency ranging from 1.5 to 2 khz (Common Mode Rejection Ratio, CMRR = 90 db; Z input = 100 MΩ; gain = 1000) 7

8 During the test sessions, the subjects will stand erect with 90 elbow flexion in the sagittal plane, upper arm by their side, palm supinated. This flexion angle will be maintained throughout the testing sessions through the use of a goniometer. The right arm will hang freely at their side. The subject will be instructed to isometrically cocontract the BB against the TB maximally for a duration of 5 seconds. Contraction time will be controlled by a digital stop watch, and an experimenter saying ready-and-flex. Following the five seconds of contraction, the experimenter will say relax. Testing will be administered on both arms with the data from the right arm serving as control measurements. Following the internally resisted contraction, an isometric MVC will be performed using external resistance. The subject s position will be the same as described above. The external resistance will be two sections of chain connected by a force transducer capable of recording forces up to the equivalent of 300lbs. One section will be bolted to the ground, while the other section will be connected to a handle. The section of chain attached to the handle will have an adjustable segment (turnbuckle) in order to maintain correct position (90 flexion, as measured by the goniometer) for all subjects. The subjects will be instructed to maximally contract the BB against the resistance of the chain. The contraction will again be for a duration of 5 seconds, controlled by the digital stop watch and voice commands. Two testing sessions will be preformed 8 weeks apart: the first test before the training, and the second test immediately following the 6-week training program. 8

9 Training The 6-week training program will consist of exclusively left-arm training exercises. The subjects will be required to attend 3 training sessions per week for the 6 week period. Eccentric, concentric, and concentric-eccentric movements will be the three types of exercise. The number of repetitions will be varied from week to week in an attempt to manipulate the intensity. The intensity will start low with low repetitions, and peak midway through the training program with higher repetitions and the assumed learned ability to co-contract. The intensity will taper off as the program concludes, in an effort to increase post-test performance as research suggests (Gibala, MacDougall, & Sale, 1994). Statistical Analysis Root mean square (RMS) of the EMG signals will be computed using the middle second of data. Using the middle second will allow for the removal of any activity build up towards a maximal contraction, as well as to eliminate any premature relaxation. The internal resistance data will then be compared to the external resistance data to give a %MVC value. The expression of the internal value as a percent of the external value will help to remove any external factors that may lead to changes in EMG over the period of the study. The pre- and post-training %MVC values will then be analyzed through a t- test to determine if any differences between the values are significant. 9

10 References Calder, K.M., & Gabriel, D.A. (2006). Adaptations during familiarization to resistive exercise. Journal of Electromyography and Kinesiology, In Press, Corrected Proof, Available online 5 June 2006, 1-8. Carolan, B., & Cafarelli, E. (1992). Adaptations in coactivation after isometric resistance training. Journal of Applied Physiology, 73(3), Chilibeck, P.D., Calder, A.W., Sale, D.G., Webber, C.E. (1998). A comparison of strength and muscle mass increases during resistance training in young women. European Journal of Applied Physiology, 77(2), Colson, S., Pousson, M., Martin, A., & Van Hoecke, J. (1999). Isokinetic elbow flexion and coactivation following eccentric training. Journal of Electromyography and Kinesiology, 9, De Luca, C.J., & Mambrito, B. (1987). Voluntary control of motor units in human antagonist muscles: Coactivation and reciprocal activation. Journal of Neurophysiology, 58(3), Farina, D., Merletti, R., Enoka, R.M. (2004). The extraction of neural strategies from surface EMG. Journal of Applied Physiology, 96(4), Gabriel, D.A., Basford, J.R., & An, K. (1997). Reversal of antagonists: Effect on elbow extension strength and endurance. Archive of Physical Medicine and Rehabilitation, 78(11), Gibala, M. J., MacDougall, J. D., & Sale, D. G. (1994). The effects of tapering on strength performance in trained athletes. International Journal of Sports Medicine, 15,

11 Nielsen, J., & Kagamihara, Y. (1994). Synchronization of human leg motor units during co-contraction in man. Experimental Brain Research, 102, Pucci, A.R., Griffin, L., & Cafarelli, E. (2006). Maximal motor unit firing rates during isometric resistance training in men. Experimental Physiology, 91, Sale, D.G. (1988). Neural adaptation to resistance training. Medicine and Science in Sports and Exercise Supplement, 20(5), S135-S145. Yanagi, T., Shiba, N., Maeda, T., Iwasa, K., Umezu, Y., Tagawa, Y., Matsuo, S., Nagata, K., Yamamoto, T., & Basford, J.R. ( 2003). Agonist contractions against electrically stimulated antagonists. Archives of Physical Medicine and Rehabilitation, 84(6),