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Thomas G. Bowman, MEd, ATC, EMT, NASM-PES, contributed to conception and design; acquisition and analysis and interpretation of the data; and drafting, critical revision, and final approval of the article. Joseph M. Hart, PhD, ATC, contributed to conception and design; analysis and interpretation of the data; and drafting, critical revision, and final approval of the article. Brian A. McGuire, MEd, PT, ATC, contributed to conception and design and drafting and final approval of the article. Riann M. Palmieri, PhD, ATC, and Christopher D. Ingersoll, PhD, ATC, FACSM, contributed to conception and design, analysis and interpretation of the data, and critical revision and final approval of the article.
Context: Muscular fatigue impedes sensorimotor function and may increase the risk of shoulder injury during activity. The effects of fatigue on the sensorimotor system of the shoulder have been studied with various results. Deceleration times have been used to study neuromuscular control of the shoulder; however, no studies involving the effects of fatigue on deceleration times have been reported.
Objective: To compare shoulder deceleration times after a shoulder internal rotation perturbation before and after a repetitive throwing exercise protocol.
Design: A 2 × 2 repeated-measures design.
Setting: Exercise and sport injury laboratory.
Patients or Other Participants: Twenty healthy, recreationally active men (age = 24.76 ± 4.03 years, height = 178.41 ± 8.36 cm, mass = 80.16 ± 15.20 kg) volunteered to participate in the study. To ensure familiarity with the overhead motion, all subjects chosen had previously participated in an overhead throwing sport.
Intervention(s): The independent variables were time (preintervention and postintervention) and session (experimental and control). The intervention consisted of continuous overhead throwing. The subjects were considered fatigued when a 10% decrease in velocity was noted on 3 consecutive pitches.
Main Outcome Measure(s): Time necessary to decelerate from an internal rotation perturbation.
Results: Deceleration time was significantly increased by the fatiguing intervention ( P = .001).
Conclusions: The decreased ability to decelerate may be an adaptive response by the subjects to dissipate a lower percentage of force per second.
The shoulder complex was the most commonly injured structure in professional baseball players between 1989 and 1999. 1 Several possible mechanisms for shoulder dysfunction have been presented, including the speed of the pitching motion, improper throwing mechanics, poor shoulder strength or conditioning, 2 and muscular fatigue. 2–5 Fatigue is believed to play a role in shoulder dysfunction because shoulder mechanics may be altered as an overhead thrower fatigues, 6 thereby decreasing the amount of force the shoulder muscles produce. 7
Afferent information about joint position sense, kinesthesia, and sensation of resistance (ie, proprioception 3) and the unconscious control of dynamic restraints to maintain joint stability during movement (ie, neuromuscular control 8) interact within the sensorimotor system to contribute to overall joint stability during activity. The central nervous system (CNS) analyzes proprioceptive information, and the proper muscular response is produced to maintain functional stability during activity. Because of the interdependence between proprioception and neuromuscular control, a decrease in one factor may decrease the other similarly. If the shoulder's ability to sense movement is altered, an altered muscular response may also result. Therefore, it is more difficult for the athlete to resist glenohumeral distraction during the deceleration phase of throwing, a mechanism of injury identified in overhead athletes from forceful eccentric contractions. 2 Either an altered sensorimotor system or fatigue may lead to increased susceptibility to injury. 2–5
Fatiguing exercises have been shown to diminish, 4, 5, 9–12 enhance, 13 or not affect 11, 13, 14 proprioception, whereas few authors have examined the effects of fatigue on neuromuscular control. 4 Therefore, it is unclear to what degree fatigue alters proprioception and neuromuscular control. These conflicts may be due to methodologic discrepancies among the studies, including differences in measurement techniques and fatiguing methods. Neuromuscular control has been assessed with only a single-arm dynamic stability test with the arm fixed against an immovable platform after fatiguing concentric internal and external shoulder exercise. A more functional measurement of the shoulder muscles' neuromuscular control, especially after a fatiguing protocol that simulates overhead throwing competition, may yield contradictory results to those found in the literature.
Gaining a better understanding of how fatigue affects the shoulder's sensorimotor system may help elucidate a potential injury mechanism in overhead throwing athletes, as fatigue is thought to play a role in shoulder dysfunction or injury. 2–5 Measuring neuromuscular control in a way that is more specific to the overhead throwing motion after a fatiguing intervention that closely simulates overhead competition may more accurately represent what happens when an overhead thrower fatigues. Therefore, the purpose of our study was to assess the change in time to decelerate the shoulder from an internal rotation perturbation after an overhead throwing protocol to fatigue.
A randomized, crossover trial design was used in this study. The independent variables were time (preintervention and postintervention) and session (experimental and control). The dependent variable was deceleration time after an internal rotation perturbation.
Twenty right-handed, healthy men between the ages of 18 and 35 years (age = 24.76 ± 4.03 years, height = 178.41 ± 8.36 cm, mass = 80.16 ± 15.20 kg) volunteered for the study. All subjects participated in an organized overhead throwing sport (eg, baseball, football) at some point in their lives. Participation could have been at any time and was intended to ensure familiarity with the overhead motion. Subjects were excluded if they reported ever having surgery on the throwing shoulder, a history of injury to the throwing shoulder within the past 2 years, or a history of cardiovascular problems or other medical conditions that would prevent their safe participation in the study. Subjects signed an informed consent form before participation as required by The University of Virginia's institutional review board, which approved the study.
Deceleration time was measured with a custom-built perturbation device similar to those described in the literature 15 (Figure 1). This device measures the shoulder musculature's reaction (time to decelerate) to a proprioceptive stimulus (internal rotation perturbation). A potentiometer, fixed along the rotational axis of the device, measured the voltage change caused by rotational movement in the device. The signal from the potentiometer was amplified at 1000 Hz and digitized by a data acquisition system (MP150; Biopac Systems, Inc, Goleta, CA) in conjunction with a personal computer. We used AcqKnowledge V.3.7.3 (Biopac Systems, Inc) to calculate the time from the initiation of the perturbation to the maximum point of internal rotation.
Internal rotation force was measured with a strain gauge load cell (model 41-tension/compression; Honeywell Sensotec, Columbus, OH) in conjunction with a digital display module (model SC200; Honeywell Sensotec) that provided real-time feedback to subjects regarding the force of their muscle contractions.
We measured pitch velocity with a radar gun (Bushnell Speedster Speed Gun; Bushnell Inc, Lenexa, KS), which was accurate to at least 1.61 kph (1 mph). Pitch velocities were measured with the lowest degree of angulation to minimize error. Each velocity was individually recorded on a data collection sheet.
The subjects participated in 2 data collection sessions, 1 experimental including the functional fatiguing protocol and 1 control in which the subjects rested for 20 minutes. We chose a 20-minute rest because we expected the experimental session to last approximately 20 minutes. The order of the data collection sessions was randomized by the flip of a coin.
The subject was positioned in the perturbation device with 90° of shoulder abduction, 90° of shoulder external rotation, and 90° of elbow flexion. He was asked to perform an internal rotation maximal voluntary isometric contraction (MVIC) while strapped into the perturbation device as the load cell measured the force of the contraction. Three trials were recorded and averaged to determine the subject's internal rotation MVIC. Twenty percent 16 of the average MVIC was calculated and used as the target force during testing. A digital force display provided visual feedback to help the subject reproduce this force accurately. As soon as the subject performed the internal rotation contraction at the target force, the perturbation device was released, causing the subject's arm to suddenly move into internal rotation. The subject was not aware of when the perturbation device would be released during the target force contraction. The release mechanism, located behind the subject, was activated while the subject was focused on the digital force display positioned in front. He was instructed to stop the internal rotation movement as quickly as possible after the release of the device and begin moving into external rotation. Three practice trials acclimatized the subject to the perturbation device during the first session. The results from 3 test trials were then averaged as baseline deceleration time.
The protocol started with warm-up pitches from a kneeling position 12 into a net approximately 10 m away. The subject was allowed to continue throwing until he felt warmed up. He was instructed to throw from the knees to help ensure that we were inducing shoulder fatigue. We did not want his core or lower extremities to fatigue, causing a decrease in pitch velocity without shoulder fatigue. The first throwing bout began with the subject continuously throwing baseballs from a kneeling position as hard as he could at a self-selected pace. He was allowed to take as much time as he wanted between pitches as long as he threw as hard as he could each time. Each throw velocity was recorded. The first throw acted as the highest velocity unless a subsequent throw was faster. Subjects threw continuously until their velocity decreased by 10% on 3 consecutive throws from the maximum velocity they were able to achieve. We chose the 10% cutoff based on the findings that collegiate pitchers' velocity drops by 3.0% 17 when they subjectively rate themselves as fatigued and professional pitchers' velocity drops by 5.5% 18 from the first inning pitched until the last inning pitched. We expected greater variations in velocity and lower overall velocities because our subjects were recreationally active; therefore, the cutoff mark was set at 10% to minimize the occurrence of a false threshold of fatigue.
The subject was then permitted a 3-minute rest before bout 2 started. The subject continued with throwing bouts, each ending when 3 consecutive pitches fell below 10% of the maximum velocity from the first bout, followed by a 3-minute rest. The functional fatiguing protocol was complete when the first 3 pitches of a bout were 10% below the maximum velocity achieved in the first bout. After the functional fatiguing protocol, the subject's deceleration time was measured in the same way as the baseline measure.
The control session included the pretest measurements of deceleration time followed by a 20-minute rest and then posttest measurements of deceleration time. The measurements were performed as described for the experimental session. The order of the data collection sessions was randomized. The 2 sessions were separated by at least 7 days if the fatiguing session was completed first; otherwise, 2 days separated the sessions. The separation was to allow the subject to fully recover from the first session before beginning the second session.
The potentiometer data were low-pass filtered at 50 Hz and 5-point smoothed. We analyzed the mean and standard deviation of a 200-millisecond time segment before the onset of the perturbation to establish an inflection point in the data (Figure 2). We defined the initiation of the internal rotation perturbation as the point of inflection at which the digital signal deviated by more than 3 standard deviations from baseline. 15 The difference in time between the inflection point and the maximum value, representing maximum internal rotation achieved by the subjects, was denoted as the deceleration time for that trial.
We calculated 2 separate 1 × 2 analyses of variance, 1 for the fatiguing session and 1 for the control session, to compare pretest with posttest deceleration times. We used version 12.0 of the SPSS statistical package (SPSS Inc, Chicago, IL) for analysis. The a priori alpha level was set at P ≤ .05.
Means and standard deviations of preintervention and postintervention shoulder deceleration times for the experimental and control sessions are presented in Figure 3. Deceleration times increased during the experimental session from the preintervention measurement (0.1817 ± 0.0300 seconds) to the postintervention measurement (0.2007 ± 0.0356 seconds). The control session yielded little difference from the preintervention measurement (0.1875 ± 0.0346 seconds) to the postintervention measurement (0.1838 ± 0.0374 seconds). The functional fatiguing protocol significantly increased the deceleration time from baseline to postfatiguing intervention (F 1,19 = 16.009, P = .001, η 2 = 0.457, 1 − β = .967). No significant difference was noted from baseline to postrest (F 1,19 = 0.804, P = .381, η 2 = 0.041, 1 − β = .136) during the control session.
Our results support the hypothesis that a functional fatiguing protocol has a detrimental effect on the ability to decelerate from an internal rotation perturbation. Our findings disagree with those of previous authors, 4 who reported no change in neuromuscular control before and after isokinetic fatiguing internal and external rotation exercise. They measured neuromuscular control with the single-arm dynamic stability test. No significant differences were found in sway velocity, but an increase in the number of touchdowns of the contralateral arm needed to maintain balance was noted. This led the authors to believe that their fatiguing intervention had a negative effect on neuromuscular control but that their measurement technique may not have been sensitive to the changes in neuromuscular control. Several possible explanations exist for the different results. We used a different fatiguing intervention that more closely simulated the events in competition involving concentric and eccentric exercising. Our measurement device did not completely simulate the dynamic throwing motion. It did, however, use a position in which the subjects' hands were freely moveable (similar to the throwing motion) to test the subjects, unlike the push-up position used previously.
In our study, the fatiguing intervention probably induced both peripheral fatigue and central fatigue, which affected deceleration time. As the musculature surrounding the shoulder joint became fatigued, muscle mechanoreceptors may have become less receptive to muscle tension and length, altering the sensory information gathered and sent or delaying transmission from the fatigued mechanoreceptor to the CNS. This theory supports the occurrence of peripheral fatigue. The mechanoreceptors most likely affected are the muscle spindles and the Golgi tendon organs, as they detect changes in muscle tension and length. 8 These “dysfunctional muscle mechanoreceptors” 10 would cause a less exact muscular response to the afferent stimulus, increasing the time necessary for the shoulder to decelerate. A transmission problem may also exist from the CNS to the motor units of the muscles providing dynamic stability. This could result in less exact movements or a delay in muscle activation. Both situations may affect humeral head positioning on the glenoid fossa because of altered biomechanics 6 or a decrease in the force 7 the dynamic stabilizers are able to generate, possibly predisposing the shoulder to injury.
It is also important to note that the changes seen may have occurred not because of neuromuscular changes but because of central fatigue. A decline may occur in the number of motor units innervated by the CNS or in the frequency of action potentials that may inhibit the muscles that provide dynamic stability. 19 Altered neuromuscular control may be a mechanism by which the dynamic stabilizers are protected from damage. 20 We speculate that taking a longer time to decelerate may decrease the amount of force per second that must be dissipated, thus decreasing the load placed on the muscle. This may help the muscles resist further fatigue by lowering their demands as the shoulder muscles fatigue. However, we cannot conclude from these data whether this adaptive response places the shoulder at risk for injury.
The fatigue induced in this study is similar to the fatigue a pitcher may experience in a game, which is a major difference between our research and the research of others 4, 5, 9–11, 13, 14 who have evaluated proprioception and neuromuscular control after fatigue. We used a 10% decrease in velocity as our cutoff for identifying fatigue to reduce the possibility of not achieving shoulder fatigue. We chose 10% because we expected our subjects to have lower overall pitch velocities and greater variances in their throwing velocities because they were not elite pitchers. The average maximum pitch speed was 84.41 ± 14.02 kph (52.45 ± 8.71 mph), much lower than would be expected of collegiate or professional pitchers. The average number of pitches thrown by the subjects to reach fatigue was 144.95 ± 46.26. Most pitchers do not throw that many pitches during a single competition; therefore, a 10% velocity decrease to define fatigue may have been slightly high. Perhaps 8% or another percentage would render results closer to predictable pitch counts for competition.
We are not surprised by the lack of a training effect as shown during the control session. The movement may have occurred too quickly for the subjects to be able to show significant improvement. Also, a limited number of trials were permitted to lessen the learning curve. Subjects were allowed practice trials to acclimate them to the device and the procedure before beginning each session. Practice trials were not permitted after the intervention, as subjects already understood the task and how to accomplish the goal of deceleration. Thus, the change in deceleration time in the experimental session may not have resulted from repeated testing.
The exact reasons for these results require further research to identify the specific structures involved in the response to fatigue. It is unclear if the deficit occurs solely during the conduction of information from the mechanoreceptors to the CNS or if a transmission problem occurs between the CNS and the muscles that elicit the response. Future researchers could also focus on whether training to resist muscular fatigue can slow the deterioration of proprioception and neuromuscular control.
The fatiguing intervention we used in this study caused a decrease in the ability of the shoulder to decelerate from an internal rotation perturbation. The control session yielded no significant differences, as subjects were able to decelerate as effectively after resting for 20 minutes. Neuromuscular changes occur when decelerating the shoulder from an internal rotation perturbation after a functional fatiguing protocol, but the exact mechanisms in the response to fatigue require further research. Although changes in the risk of injury cannot be concluded from these data, clinicians who are aware of these neuromuscular and proprioceptive changes may make better decisions regarding the participation of athletes in repetitive overhead activities while fatigued.