The most common adaptation that is seen clinically in throwers is a shift in the arc of shoulder motion bilaterally. Throwers often present with a decrease in glenohumeral internal rotation (IR) and a concurrent increase in glenohumeral external rotation (ER) on the throwing arm compared to the nonthrowing arm [49–58] (Fig. 1.2). Wilk et al. [41] has developed the total motion concept which adds IR and ER together to calculate the total arc range on each side. Wilk et al. [41] states that if the total motion is equal bilaterally regardless of the shift in motion pattern, then the clinician should not be concerned. When total motion is equal bilaterally, it has been suggested that the shift in the arc of motion is only caused by a bony adaptation called humeral retroversion. However, if there is a loss of total motion on the throwing side, there is usually a soft tissue tightness present which may be reversible with treatment. Recently, this has been supported demonstrating that baseball players with a loss of total motion of 5° or more had a higher rate of shoulder injury [59, 60]. In addition to the total motion concept, there has been much research investigating glenohumeral internal rotation deficits (GIRD) . This is a term that has been developed to describe the loss of IR on the throwing arm [52]. There are several hypotheses for the cause of GIRD; however, evidence is still lacking to fully understand the specific tissue adaptations. The three main hypotheses are humeral retroversion, posterior rotator cuff tightness, and posterior capsule tightness/thickness. Each of these tissue adaptations will be discussed in detail in upcoming sections. Regardless of the source of GIRD, it was demonstrated that baseball players with a GIRD of 20° or more were two times more likely to be injured [59].

The bone is a tissue that is known to have adaptable properties to mechanical load [61]. As such, throwing causes several bony adaptations that are important in understanding the throwing athlete. First, humeral retroversion is described as the bony rotation between the proximal and distal ends of the humerus [62] (Fig. 1.3). Traditionally, it is measured with CT or MRI; however, ultrasound has been demonstrated to be as accurate and have much more accessibility [63, 64]. To understand humeral retroversion in throwers, we first need to discuss the developmental process in normal individuals. At birth, the humerus is in an excessively retroverted position [65]. Clinically this equates to increased glenohumeral ER and decreased glenohumeral IR [66]. Throughout normal development, the humerus undergoes a rotation process that decreases the amount of humeral retroversion. It has been shown that 80 % of the normal developmental rotation process is completed by 8 years old and the remaining 20 % extends to 18 years old [65]. Throwing prior to the completion of this normal developmental rotation process seems to diminish or halt the process, thereby creating side to side differences in humeral retroversion. Most throwers will have more humeral retroversion on the throwing side compared to the nonthrowing side. The association between humeral retroversion and injury is still being heavily researched. Initially, it was suggested to be a positive adaptation. Early researchers reasoned that increase retroversion would afford ER without stretching the anterior capsule and would theoretically inhibit tuberosity/glenoid contact in ER (internal impingement) [47]. However, some recent research suggests that baseball players with greater humeral retroversion have a history of elbow injury [67]. Others have found that baseball players with greater humeral retroversion have a thicker posterior capsule of the shoulder [68], which has been implicated in causing shoulder and elbow injuries [52]. Currently, the evidence suggesting that humeral retroversion is either helpful or deleterious to long-term performance is inconclusive.

Next, bone mineral density has been examined bilaterally in baseball players. The results of these studies suggest that the proximal and mid shaft of the humerus on the throwing arm has increased bone mineral density [69, 70]. This finding would be hypothesized based on Wolf’s law [61] and the rotational stress of throwing. These results suggest that throughout development, the humerus will adapt in a manner equal to the mechanical loads that are placed on it. This information is important in adolescent throwers due to the open epiphyseal plate at the proximal humerus and the increased propensity for little leaguer’s shoulder. Adolescent throwers need to progress in throwing at a much slower pace and also limit the amount of pitches per game and season to allow the bone to adapt at a healthy rate.

The last bony adaptation that can occur in throwers is morphological changes to the bicipital groove. The bicipital groove can develop stenosis from bone ingrowth or spurs [71] (Fig. 1.4). The increased growth of bone within the groove will cause mechanical irritation to the synovial sheath of the biceps tendon and over time cause significant injury. Although bicipital grove stenosis hasn’t been documented much in the literature, it likely occurs more frequently in throwing athletes than has previous been suspected.

There are many different types of soft tissues in the shoulder that can adapt due to the stress of throwing. Each tissue is different in terms of its composition, structure, and function. In this section, we will discuss all of the different types of soft tissue that are important when treating throwing athletes.

The first category is the joint capsule . The capsule is composed of an inner and outer layer. The inner layer is known as the synovial layer and is responsible for secreting synovial fluid to maintain joint health. The outer layer is composed of dense irregular connective tissue [72]. This layer provides the strength and stabilizing component to the capsule. Throwers can develop adaptations in both the anterior and posterior locations of the joint capsule [68, 73]. During the late cocking and acceleration phase of throwing, large anterior forces occur [14]. Due to these repetitively large forces, it is often thought that the connective tissue of the capsule plastically deforms and is left in a lengthened position. Structurally, the anterior capsule will be unable to center the humeral head on the glenoid at the end ranges of motion. This will allow increased joint translations in the anterior direction, which has been thought to cause secondary impingement or labral injury [74]. During throwing, the athlete will have excessive ER and pain during the late cocking phase of the throw. However, a detailed examination is necessary to discern whether the ER seen during throwing is caused by a combination of glenohumeral, scapular, thoracic, and lumbar motion. It is important to note that anterior capsular laxity does not occur to every throwing athlete. It is often used as a generic diagnosis due to the player having excessive ER and shoulder pain. For example, a recent study by Borsa et al. [75] demonstrated that healthy college throwers did not have side to side differences in anterior translation. This suggests that when this increased anterior humeral translation does occur, it is likely pathologic and may require surgical intervention.

Next, the posterior capsule also undergoes structural adaptations; however, these adaptations are much different than the anterior capsule. When examining pitching kinetics, research has shown that during the deceleration phase, the distraction force is on average 1.5 times body weight [14]. Typically, during the deceleration and follow-through phase, the posterior rotator cuff muscles and scapular stabilizers can absorb the energy [76]. However, throughout a game, these muscles will likely fatigue, thereby reducing the amount of energy that can be absorbed [77]. In this situation, the shoulder will continue to internally rotate to the end range, which will place the remaining force on the posterior capsule. According to Wolf’s law [61], the posterior capsule may adapt to the increased stress by hypertrophying. It has been hypothesized that the posterior capsule will ultimately become thick and fibrotic with repetitive throwing, which will create noncompliant tissue and limit glenohumeral IR. Thomas et al. [68] has measured this thickness with ultrasound and found that the throwing shoulder’s posterior capsule is thicker compared to the nonthrowing shoulder and the thickness correlates with the loss of glenohumeral IR. In addition, several cadaver studies have shown that a tight posterior capsule will shift the center of the humeral head in a posterior-superior direction during the late cocking phase of the throw [78, 79]. A posterior-superior shift of the humeral head has been demonstrated to cause internal impingement and place increased stress at the insertion of the long head of the biceps tendon at the superior labrum [52] (Fig. 1.5). It is expected that the posterior capsule thickens due to throwing; however, it is currently unknown when this adaptation becomes excessive and problematic.

The next category of soft tissue that is a concern with throwers is muscle/tendon units. There are several muscle/tendon units that develop similar adaptations at the shoulder girdle. The muscles that will be discussed include the posterior rotator cuff (infraspinatus and teres minor), pectoralis minor, triceps brachii, latissimus dorsi, and the teres major.

First, the infraspinatus and teres minor are the two muscles that comprise the posterior rotator cuff. As stated previously, these two small muscles attempt to repetitively absorb a large amount of the 1.5 times body weight force that occurs during the deceleration phase of the throw [14]. To absorb energy, muscles function eccentrically which entails a forceful breaking of the myosin and actin bonds [80]. Several studies have found that repetitive eccentric contractions of the muscle cause significant damage, often called delayed-onset muscle soreness (DOMS) [81–83]. Several studies have also identified that repetitive eccentric contractions cause an increase in passive stiffness and reduced range of motion that peaks at 24 h and typically takes 4–5 days to return to baseline [84, 85]. It is hypothesized that this clinical presentation is caused by damaging of the sarcoplasmic reticulum, which releases excessive calcium [84]. This has been demonstrated in throwers following a simulated game and is characterized by a decrease in glenohumeral IR immediately following the game [86]. Recently, it has been shown that the loss of IR is still present up to 3 days following pitching [87]. This physiologic phenomenon of muscle would not be a concern if throwing did not occur until after the muscle tissue returned to a normal state. However, most throwers initiate throwing before the muscle tissue returns to normal. Over time, the posterior rotator cuff muscles may develop excessive tightness. The hypothesis is that the immediate loss of glenohumeral IR following throwing will still be present before the next bout of throwing, thereby adding to the total loss of motion. This can continue to occur over the season leading to excessive tightness, characterized by a loss of glenohumeral IR. Posterior rotator cuff tightness is thought to be problematic and is hypothesized that it will alter normal throwing biomechanics [52]. During normal throwing, the shoulder is positioned in the scapular plane (30° anterior to the frontal plane) during the late cocking phase [1, 88]. A tight posterior rotator cuff may position the shoulder in the frontal plane or even in excessive horizontal abduction to release the tension in the posterior rotator cuff. This position will place increased valgus stress on the medial elbow and increased anterior stress on the anterior capsule and cause internal impingement [15, 89]. To address this situation, clinicians should focus on treating the excessive posterior rotator cuff tightness [90–92] and not attempt to change the altered throwing biomechanics. As the muscle tightness is resolved, the altered biomechanics will return to normal.

There are additional muscles that are often overlooked in throwing athletes but do develop significant tightness that can affect throwing biomechanics. The next group of muscles includes the pectoralis minor, triceps brachii, latissimus dorsi, and the teres major. One commonality of these muscles is that they have an attachment on the scapula and therefore can have an effect on scapular motion. The latissimus dorsi is one exception to that rule, but the research isn’t entirely clear. According to most anatomy textbooks, the latissimus dorsi does not have a common attachment site on the scapula, although one cadaver study did recognize that 40 % of the cadavers had an attachment to the tip of the inferior angle [93]. However, the age of the cadavers was not reported, and the attachment may have developed as an adhesion due to patients being bedridden. Future research should identify the prevalence of this attachment in overhead athletes. The pectoralis minor is a thin broad muscle that originates at the third to fifth ribs and inserts on the coracoid process of the scapula. The muscle functions to depress and protract the scapula, although it does not create large ranges of motion. Throwing athletes commonly develop excessive tightness of this muscle with unknown origin [94]. It is thought that the tightness corresponds with inhibition/weakness of the posterior scapular stabilizing muscles, such as the lower trapezius and rhomboids [95]. Since serratus anterior inhibition/weakness is often observed [96, 97] and is the major scapular protractor, pectoralis minor tightness might develop due to compensation for the serratus anterior during throwing. Regardless of the mechanism, pectoralis minor tightness will cause excessive scapular protraction and anterior tilting at rest and during overhead motions [98]. This position has been shown to decrease the subacromial space, which increases the likelihood of developing subacromial and subcoracoid impingement [99]. It also can cause increased anterior stress on the anterior capsule during the late cocking phase of throwing [100]. Stretching is often difficult due to the anatomy of the pectoralis minor, and preventative stretching is likely more effective than waiting until tightness develops [101, 102]. Next, the triceps brachii has a broad origin due to three heads; however, the long head originates on the inferior glenoid and inserts with the other two heads distally on the olecranon process. Therefore, the long head of the triceps brachii is a two-joint muscle and functions at both the elbow and the shoulder. The triceps is very unique since it must coordinate motion at both the shoulder and elbow simultaneously during throwing. This is especially important during the deceleration and follow-through phase of the throw when the muscle is functioning eccentrically to absorb energy. Since the triceps must stabilize and absorb energy at two joints, the stress will be increased within the muscle, thereby creating more eccentric muscle damage during throwing. Similar to the posterior rotator cuff, the triceps will also experience an increase in passive muscle tension and reduced range of motion that requires 4–5 days to recover [85, 103]. Throwing prior to complete recovery will cause the triceps to continually develop tightness throughout the season. Triceps tightness will directly affect scapular motion since its origin is on the inferior glenoid. When the triceps is tight, it has the potential to pull the scapula into excessive protraction and anterior tilting during the deceleration and follow-through phase of throwing. This will cause excessive eccentric loading on the scapular retractors and serratus anterior, which are muscles that often develop inhibition/fatigue. In addition, triceps tightness also has the potential to decrease glenohumeral IR due to the origin on the inferior glenoid. As previously stated, GIRD can be caused from various sources (bone, capsule, posterior rotator cuff, and triceps) and can increase the likelihood of injury [59]. Examining for triceps tightness involves measuring elbow flexed and elbow extended forward flexion with the scapula stabilized [104]. If there is a large increase in forward flexion with the elbow extended, then the loss of motion is caused by triceps tightness. The final group of muscles to be discussed is the internal rotators. Throwing athletes typically have very strong internal rotators [105], which allow them to throw with high velocities. However, the overdevelopment of these muscles often causes excessive tightness. The two major internal rotators that develop adaptive tightness are the latissimus dorsi [106] and the teres major [107]. Both muscles share a common insertion site on the medial aspect of the bicipital groove of the humerus and therefore will affect glenohumeral motion in a similar way when tight. Tightness of these muscles will limit forward flexion and glenohumeral ER. During the late cocking phase of the throw, ER is essential to impart maximal velocity [2, 108]. Typically the thrower is still able to achieve normal ER by compensating at other locations. First, tightness within the latissimus dorsi may cause an excessive lordotic curve within the lower back to ultimately achieve the same glenohumeral ER [31, 106]. Second, tightness within the teres major can directly affect scapular motion [109] to ultimately achieve the same glenohumeral ER, further contributing to the inhibition/weakness of the scapular stabilizers. The tightness can be assessed clinically by examining forward flexion and glenohumeral ER with the scapula stabilized. Stabilizing the scapula is important to isolate the muscular tightness since the scapula can often compensate. The teres major does have a direct attachment on the scapula, making stabilization very important. The latissimus dorsi may have an attachment on the scapula, but it is still debatable. Tightness of the internal rotators has not been greatly recognized in the literature, and therefore, the association with shoulder and elbow injuries is not known.