AMERICAN SOCIETY OF BIOMECHANICS
Presented at the Twenty-First Annual Meeting
of the American Society of Biomechanics
Clemson University, South Carolina
September 24-27, 1997
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| AMERICAN SOCIETY OF BIOMECHANICS
Presented at the Twenty-First Annual Meeting |
Lateral Epicondyle Tendonosis, or common tennis elbow, afflicts many tennis players. Work in the past has examined many biomechanical and electrophysiological parameters associated with playing tennis (Bernhang et al. 1974) Some recent work by Kelly et al. (1994) has even evaluated EMG for players suffering from tennis elbow. This study was conducted to determine if the muscle firing patterns of the racket arm extensors, flexors and triceps muscles were similar between matched groups of healthy and tennis elbow suffering players.
Tennis elbow afflicts between 30% and 50% of all tennis players (Priest et al., 1980). The injury is usually the painful result of microtrauma to the Extensor Carpi Radialis Brevis caused by the excessive eccentric loading experienced while hitting backhand shots. The microtrauma eventually presents itself as pain in the lateral aspect of the elbow and persists as long as the person continues to play. With rest the condition usually disappears, however, in extreme cases surgery may be required to relieve the pain. It is our theory that the pain of this injury induces a shift in normal muscle activation patterns which is detrimental to the healing process. The muscles need to rest for healing to occur, while our observations indicate that muscle activation actually increases while playing tennis when suffering from tennis elbow. This change in the activation patterns increases the severity of the injury and prevents healing.
This study was conducted to quantify the amount of racket arm EMG activity by providing a profile of the temporal characteristics of muscle firing with respect to ball/racket impact. The hypothesis tested was that injured players would display longer muscle activation duration for the selected muscle groups for the same impact conditions when compared to their healthy counterparts.
Eight male tennis players were selected for this study. Four of the players had been clinically diagnosed as suffering from tennis elbow at the time of their participation in the study. Each of the subjects signed an informed consent form prior to testing. A one-handed backhand block volley was the tennis shot evaluated. Nine impact conditions were randomly presented to the subjects during testing. The impact conditions were selected to simulate the variety of impacts experienced during normal tennis play. The nine conditions consisted of all possible combinations of three racket face impact locations and three impact velocities. The impact locations were: 1. Center (C), the geometric center of the racket face, 2. Long Axis (L), location found at 8 cm from the end of the racket and 3. Torsional, (T), located 7 cm from the top side of the racket when held oriented with the face perpendicular to the floor and the grip parallel to the floor. The three impact velocities were: 1. Slow (S) 12m/s, Medium (M) 17m/s, and High (H) 23m/s. The tennis balls were projected by a ball machine at the stationary hand-held racket at a distance of 2m. EMG surface electrodes were placed over the Extensor (E), Flexor (F) and Triceps (T) of the subject's racket arm. EMG data were collected at 1000Hz. An accelerometer attached to the racket throat provided a signal synchronized with the EMG recordings which was used to determine the instant of impact. All trials were video taped and this information provided a visual method of selecting which impact data would be analyzed. Data were collected in nine 30 second trials during which the subject typically struck eight shots. None of the first two shots per condition were used for analysis purposes. For this study three good impacts for each condition were selected for analysis. A good impact was defined as one which struck the selected racket face location while the racket was oriented properly. Muscles were considered active if the magnitude of EMG reached 20% or greater of that recorded during maximum voluntary muscular contractions conducted prior to the start of the experimental trials.
Data were analyzed by determining the on/off conditions of the muscles within a 2000ms window bounding impact. This allowed study of which muscles were active during the 1000ms prior to impact and 1000ms following ball/racket impact.
Single factor ANOVA's with p = 0.05 were performed to determine significant differences for subject health status (Injured or Healthy) vs. muscle activation times for the all impact conditions.
Analysis of the data indicate that the Extensor muscles were activated significantly earlier (p < 0.05) for the Injured subjects than for the Healthy subject group. Additionally, the Extensors were active longer after impact in the Injured group than in the Healthy subjects (p<0.05). The other muscle groups tested, Flexors and Triceps, showed no statistically significant differences in activation between the two subject groups either before or after impact (p >0.05). Figure 1 illustrates the average time of muscle activation prior to impact for the subjects tested. The muscle activation patterns following impacts are shown in Figure 2.
The analysis indicates that the injured and healthy groups do not use identical activation patterns of racket arm musculature with respect to similar ball/racket impacts.
Figure 1: Illustration of muscle activation duration prior to all impact conditions.
Figure 2: Illustration of muscle activation duration following all impact conditions.
While other groups have used EMG to study tennis strokes, none have directly compared the muscle activation sequencing and activation duration of both healthy and injured players under various impact conditions. Results indicate a need to educate players suffering from tennis elbow about the injurious muscle activation strategies which develop once pain is present and the need to develop therapeutic or motor learning strategies which will help the players speed the healing process instead of promoting the duration and severity of the injury.
Bernhang, H.B. et al., J. Sport Med., 2, 235- 260, 1974.
Kelly, J.D. et al., Am. J. Sport Med., 22(3), 359- 363, 1994.
Priest, J.D. et al., Phys. Sport Med. 8(4), 80-91, 1980.
I would like to thank the following people and companies for their support: Robert Murray, the Penn State Biomechanics Laboratory , Paromed Medzintecknik, Germany.
