The throwing motion in the overhead-throwing athlete, such as a baseball player, is a complex biomechanical phenomenon. This highly skilled movement, performed at extreme velocities, requires a delicate combination of flexibility, strength, coordination, synchronicity, and neuromuscular control. The athletes' throwing shoulder must exhibit adequate dynamic stability that provides sufficient mobility to accommodate the throwing motion, while preserving stability needed to prevent symptoms and/or injury.1
In previous studies,2–5
altered mobility patterns have been reported in the throwing shoulder of baseball players, especially when compared to the non-throwing shoulder. The throwing shoulder typically presents with hypermobility in some directions while demonstrating hypomobility in others. This atypical mobility pattern may be attributed to the structural changes found in the glenohumeral joint capsule, labrum, rotator cuff musculature, ligaments, and osseus structures that occur in response to the demands of overhead throwing. The throwing motion used in baseball requires the arm to be forcefully propelled forward from a position of full external rotation to near full internal rotation. The posterior rotator cuff must act in an eccentric fashion to decelerate and control the arm as it internally rotates and horizontally adducts across the body.6
Previous authors have suggested that the throwing shoulder typically exhibits increased external rotation and decreased internal rotation when compared to the non-throwing shoulder. This loss of internal rotation in the throwing shoulder is defined as the glenohumeral internal rotation deficit (GIRD).7
Both soft tissue and osseous tissue changes have been linked to GIRD. Increased external rotation and decreased internal rotation in the dominant extremity have been correlated with an increase in humeral retroversion.8
From a soft tissue perspective, asymmetric capsular tightness (especially posterior tightness) has also been suggested as a cause of the observed loss of internal rotation.7
In a study by Burkhart, et al, evidence was presented to support the prediction that asymmetric glenohumeral capsular tightness could contribute to a wide variety of pathologies.9
As a result of Burkhart's work, those who care for pitchers in professional baseball have begun to develop stretching programs to address internal rotation deficits. These programs have been reported to be effective at reducing innings lost and surgical procedures performed on the throwing shoulder of professional pitchers.10
Craig Morgan, MD explained the concept known as the pathological cascade
of the throwing shoulder. He stated that the first sign of shoulder pathology is a painless loss of velocity and command caused by an early loss of glenohumeral internal rotation secondary to a posterior capsule contracture. Once this cascade has begun, the GIRD will cause the posterior inferior capsular contracture to become progressively less mobile. This increased posterior tightness, Morgan asserted, would lead to posterior shoulder stiffness and an inability to properly prepare for competition.11
Progression of the cascade includes a third stage that presents as posterior shoulder pain without mechanical symptoms. This pain is felt during the late cocking and early acceleration phases of the throwing cycle due to posterior superior glenohumeral instability. The posterior inferior capsular contracture forces the humerus into a posteriorly and superiorly shifted position, adding undue strain on the posterior superior labral-glenoid complex. This posterior superior shifting allows an increase in external rotation that places the posterior superior rotator cuff in position to contact the glenoid margin resulting in symptoms of internal impingement. The contracture and resultant posterior superior shift lead to the development of mechanical symptoms usually evident in the late cocking and early acceleration of the players throwing phase, representing the fourth stage of the cascade. These symptoms occur due to the subsequent failure of the bicep and posterior superior labrum anchor, secondary to the capsular contracture.11
This loss in anchoring tension on the glenoid attachments allows anterosuperior translation of the humeral head during forced humeral elevation and internal rotation, as seen with overhead throwing, leading to the “SLAP event” (Superior Labral Anterior-Posterior) and subsequent tearing of the posterior superior labral rim.12
According to Morgan, the SLAP event can be avoided by initiating posterior capsular stretches early in the cascade to eliminate contracture. Once the SLAP event has occurred, mechanical symptoms most often become a surgical issue. As the player continues to throw through these symptoms, subacromial and rotator cuff symptoms will develop.11
In some cases of GIRD there may be no increase in external rotation. In these cases there exists a likelihood of pathological internal impingement. Myers et al stated that throwers with pathologic internal impingement will exhibit significantly increased posterior shoulder tightness and glenohumeral internal rotation deficit without significantly increased external rotation gain.13
Based on the review of the related literature, the authors of the current study decided to assess the glenohumeral internal and external rotation range of motion of the shoulders of NCAA Division I baseball players.
Therefore, the two specific purposes of this research were: 1) to determine the prevalence of glenohumeral internal rotation deficit in the sample of Division I collegiate baseball players , and 2) to determine the effectiveness of a twelve-week posterior capsule stretching program on GIRD.
The authors hypothesized that the posterior capsule stretching program would statistically improve the internal rotation measures over a twelve week period.