The upper extremity is one of the most frequently injured regions in tennis players. In the 2013 ATP World Tour, shoulder injuries (10 % of all injuries) were in fourth position after spine (26 %), thigh muscles (13 %) and foot/ankle (11 %) injuries. Sallis et al. found that there is no significant difference in injury rate between men and women [4]. The most common diagnosis in tennis players with shoulder pain are ‘impingement’ and ‘rotator cuff and long head of the biceps tendonitis’, frequently due to ‘overuse syndrome’ (chronic injuries). This syndrome could result from kinetic chain dysfunction, scapular dyskinesis and glenohumeral internal rotation deficit (GIRD). In case of kinetic chain dysfunction and scapular dyskinesis, the shoulder joint becomes the victim and not the culprit of a dysfunction, eventually resulting in an anatomical injury with clinical findings affecting the shoulder girdle. This kind of approach might explain the failure of some surgical ligament and tendon repair techniques, too often attributed to failed materials (anchors, suture, bio- and not reabsorbable material) or local biological factors (vascularization, fatty infiltration, etc.) forgetting that these anatomical lesions are often the end point of a failure in the kinetic chain that, if not correct, may inevitably reproduce the lesion over time, even after surgery. The dynamic scapulothoracic stability and the importance of the core stability give the ideal hint to understand those mechanisms that when altered can lead to shoulder dysfunction. The shoulder is a complex mechanical structure containing several joints connecting the humerus, the scapula, the clavicle and the sternum. The scapula slides over the dorsal part of the thorax; it can glide over the so-called scapulothoracic gliding plane. It is a closed chain mechanism. The relation between the rotations of the humerus and scapula is commonly referred to as the scapulohumeral rhythm. The scapular motion strongly affects the mechanical energy delivered by the muscles and the metabolic cost required to obtain the desired force. At the same time the scapula has different roles being a functional part of the glenohumeral joint, retracting and protracting along the thoracic wall and elevating the acromion. It is a site for muscle attachment and a link in the proximal to distal sequencing of velocity, energy and force that allows the most appropriate shoulder function [5]. The core is where the centre of gravity is located and where movement begins. An efficient core allows for maintenance of the physiological length–tension relationship of functional agonists and antagonists and for normal force couple in the lumbo-pelvic hip complex. The musculoskeletal core of the body includes the spine, the hips, the pelvis, the proximal lower limb and abdominal structures; muscles of the trunk and pelvis are responsible for the maintenance of stability of the spine and are critical for the transfer of energy from large to small body parts during many work/sports activities. The roof of the core muscle structures is the diaphragm. At the opposite end of the trunk component of the core muscles are the pelvic floor muscles. Core muscles have large cross-sectional areas and generate a great amount of force and power for athletic activities. The thoracolumbar fascia is an important structure that connects the lower limbs (via the gluteus maximus) to the upper limbs (via the latissimus dorsi). Function, the end result of the kinetic chain, can be defined as optimal anatomy acted upon by physiological muscle activations to produce optimal biomechanical forces and motions. Core stability is essential for the maximum efficiency of the shoulder function. A functional definition of ‘core stability’ is the ability to control the trunk over the pelvis to allow the coordinated sequenced activation of body part to produce, to transfer and to control force and motion to the terminal segments in integrated body activities, to obtain the desired work/athletic task [6]. This definition implies patterned sequences for force generation and transfer, proximal stability for distal mobility and control in three dimensions. Core muscle activation is used to generate rotational torques around the spine and provides stiffness to the entire central mass, making a rigid cylinder that confers a long lever arm around which rotation can occur and against which muscles can be stabilized as they contract [7]. One of the most important abnormalities in scapular biomechanics is actually the loss of the ‘link function’ in the kinetic chain; if the scapula does become deficient in motion or position, transmission of the large generated forces from the lower extremity to the upper extremity is impaired. This creates a deficiency in resultant maximum force that can be delivered to the hand or creates a situation of ‘catch up’ in which the more distal links have to work more actively to compensate for the loss of the proximally generated force. This can impair the function of the distal links because they do not have the size, the muscle cross section area or the time to efficiently develop these larger forces. Kibler calculations have shown that a 20 % decrease in kinetic energy delivered from the hip and trunk to the arm necessitates an 80 % increase in mass or a 34 % increase in rotational velocity at the shoulder to deliver the same amount of resultant force to the hand [5]. This required adaptation can cause overload problems with repeated use. In condition of sport-related stress, regulatory imbalance might result both in typical reaction patterns and individual response specificity; this can explain the anatomo-pathological difference of several lesions (extension, site, degrees of retraction, etc.), and it justifies those clinical pictures that even if triggered by similar lesions appear at different times and with different clinical features.

Repetitive concentric and eccentric demands on the rotator cuff and hypermobility and excessive laxity of the glenohumeral joint could lead to scapulothoracic muscular fatigue altering the normal shoulder biomechanics. Fatigue affects sensation of joint movement, decreases athletic performance and increases fatigue-related shoulder dysfunction. The muscular imbalance during the deceleration phase transfers distraction forces to the posterior capsule that becomes tight and leads to an internal rotation reduction (glenohumeral internal rotation deficit or GIRD). Posterior capsule tightness may be forcing the humeral head forward, causing mechanical impingement and a loss of range of motion as a result of the avoidance of painful movements. Although the factors contributing to secondary shoulder impingement are multiple, the posterior capsule tightness is thought to alter shoulder kinematics, with superior translation of the humeral head during flexion such that the rotator cuff is compromised by the overlying coracoacromial arch. Glenohumeral joint tightness can also create abnormal biomechanics of the scapula. Posterior shoulder inflexibility, due to capsular or muscular tightness (infraspinatus thixotropy), affects the smooth motion of the glenohumeral joint and creates a wind-up effect so that the glenoid and scapula actually get pulled in a forward and inferior direction by the moving and rotating arm [8]. This can create an excessive amount of protraction of the scapula on the thorax as the arm continues into the horizontally adducted position in follow through. Because of the geometry of the upper aspect of the thorax, the more the scapula is protracted in follow through, the farther it and its acromion move anteriorly and inferiorly around the thorax. In all cases with suspected impingement, a careful examination of both passive and active motion of the shoulders in all planes is needed. In those patients with limited internal rotation and flexion, a therapy programme should be directed at improving these motion planes.

The abnormal scapular biomechanics, occurring as a result of dysfunction, create an abnormal scapular position that decreases normal shoulder function and exposes the shoulder to injury if prevention strategies are not applied. The most common shoulder lesion in tennis players are ‘superior labral tears (SLAP)’ and ‘rotator cuff tears’. Posterior or posterior superior shoulder pain is felt without mechanical symptoms usually described as occurring during the late cocking and early acceleration phases of the throwing cycle. This is due to posterior superior glenohumeral instability directed by the posterior inferior capsular contracture as the shoulder abducts and rotates. The posterior superior shift of the glenohumeral contact and rotational point creates strain on the posterior superior labral glenoid interface as well as allows for increased external humeral rotation which brings the undersurface of the posterior superior rotator cuff in contact with the posterior superior glenoid margin resulting in the early symptoms of internal impingement. The SLAP event occurs when the posterior superior labrum and biceps anchor fail in tension from their glenoid attachments secondary to the capsular contracture mediated by posterior superior glenohumeral instability. Once the SLAP event has occurred, the thrower promptly develops mechanical symptoms in late cocking and early acceleration phases. Once mechanical symptoms appear, the problem becomes surgical and will not be improved or solved conservatively. Conversely, prior to the slap event, the symptomatic throwing shoulder can usually be successfully treated by a series of focused posterior inferior capsular stretches to eliminate the contracture and strength exercises to rehab any concomitant rotator cuff- and scapular stabilizer-deconditioned musculature. After the development of mechanical symptoms of the SLAP lesion, if the thrower continues to throw, subacromial and rotator cuff symptoms ensue due to contracture-mediated increasing posterior superior glenohumeral instability with secondary subacromial space restriction and increasing internal impingement events. This can lead the athlete, in the course of time, to a rotator cuff tear that have to be fixed arthroscopically.

Injuries to the elbow region in elite tennis players primarily involve repetitive overuse and centre on the tendonous structures inserting at the medial and lateral humeral epicondyle [9]. The reported injury rates for tennis elbow are quite high, with percentages ranging from 37 to 57 % in elite and recreational players. Nirschl and Sobel also show higher rates of incidence in elite players on the medial side of the elbow from overload on the serve and forehand strokes compared with higher rates of lateral humeral epicondylitis in lower-level recreational players from the overload on the backhand ground stroke [10]. The most frequent injuries in professional tennis player occur on the medial side of the elbow such as medial epicondylitis and medial instability due to ulnar collateral ligament lesion (UCL lesion), a result of chronic overuse. When acute injuries do occur, they are the result of a traumatic event. With increased training, players may experience muscle fatigue. Due to this reason changes in mechanics placing could increase strain on the UCL. Muscular fatigue may lead to a decreased shoulder abduction angle that has been shown to place greater force on the medial elbow [11]. Chronic overuse leads to microtrauma and attenuation of the ulnar collateral ligament. Traction spurs and calcification on the UCL are common radiographic signs of repeated injury on the medial side of the elbow. Progressive attenuation of the ligament ultimately results in an incompetent ligament and forms part of the continuum leading to valgus extension overload that ends with a medial instability. Players typically do not experience limitations until trying to serve beyond 75 % of the full potential. Pain is most commonly reported during the late cocking and early acceleration phases of serving. Players with UCL insufficiency could have symptoms involving the ulnar nerve, resulting of traction, compression or irritation from the surrounding inflammation in the setting of an incompetent UCL. The exercises recommended for prevention of elbow injury focus on increasing the strength and particularly the muscular endurance of the wrist and forearm musculature. It is important to note that contrary to common beliefs among coaches, players and even medical professionals, power generation does not come from the wrist and forearm in properly executed tennis strokes. Instead, the summation of forces from the entire body or kinetic chain produces the power that is transferred through the wrist, forearm and ultimately to the racquet head to generate power [12, 13]. Reliance on the forearm musculature for power generation is a common clinical hypothesis for the origin of elbow pathology in tennis players due to nonoptimal contributions from other segments of the kinetic chain and poor overall stroke biomechanics and whole body fitness [14].