The modern tennis game is based around power and high ball velocity, resulting in repetitive stress loads and high-energy forces on the body leading to both traumatic and overuse injuries (1). Adding to injury risk are changes in racquet technology and game style from shorter serve and volley game play to longer heavy baseline rallies (1).
Injury surveillance in elite tennis has historically been lacking, variable, and nonuniform in its reporting (2,3). To address these shortcomings and to establish more consistent tennis-related injury data reporting, a consensus statement was established to determine uniform definitions and methodologies (3). This has led to an increase in epidemiology studies with injury reports from the US Open, Australian Open, Wimbledon, Davis Cup, the Women's Tennis Association (WTA), and the Association of Tennis Professionals (ATP) (2,4–8).
Epidemiology reporting discrepancies still exist, especially around the definition of injury exposure where a variety of definitions are used: per 1000 h, per 1000 matches, per 1000 sets, per 10,000 matches (3,5,7,8). This variability may potentially influence the data in these studies.
The objective of this article is to review the current epidemiology injury surveillance data on elite players to discern the common upper limb injuries these athletes sustain. Furthermore, we will review less well-known upper-limb injuries that are not frequently reported yet are frequently encountered, as determined by a sports medicine physician with significant experience working with elite tennis players.
Materials and Methods
To establish exposure rates, injury regions, and types in tennis players, a search was conducted for epidemiology studies involving elite tennis players. Seven studies were selected and reviewed including injury surveillance studies from the US Open, Australian Open, Wimbledon, Davis Cup, WTA, and ATP. A list of common injuries in the upper limb was then comprised and subsequently reviewed by TW, an expert in tennis injuries and Australian Open Chief Medical Officer from 2001 to 2017. The list was refined to the most common injuries of the upper limb with the addition of less well known yet clinically relevant injuries. Biomechanical studies, where available, were then reviewed to help establish the potential tennis biomechanical etiology and management of each injury.
Higher injury exposure rates in women compared with men were recorded both at the Australian Open (201.7 and 148.8 per 10,000 games) and Wimbledon (23.4 and 17.7 per 1000 sets), conversely the US Open reported higher exposure rates in men (48.1 and 40.64 per 1000 h) (5,7,8). Injury by region was consistent across the studies and sexes with lower-limb injuries accounting for approximately 40% to 47%, upper limb 20% to 28%, and the trunk for 8% to 16% of all injuries (2,4,5,7,8). Acute injuries were reported higher than chronic injuries at the US Open (27.65 and 19.51 per 1000 h), inversely chronic injuries were higher than acute at Wimbledon (52% and 48%). Acute injuries are more prevalent in the lower limb, while overuse injuries are more common in the upper limb. Muscle strains and tendinopathies are the most prevalent injury in both men and women, while injury sites common to men and women include, knee, thigh, low back, shoulder, wrist, and foot (2,4). The prevailing upper-limb injuries in men are internal shoulder impingement, superior labrum anterior and posterior (SLAP) tears, elbow tendinopathies, and extensor carpi ulnaris (ECU) tendinopathies/subluxation, whereas in women shoulder tendinopathy was the most prevalent upper-limb injury (2,4).
Posterior shoulder instability
Posterior shoulder instability accounts for approximately 5% of cases of glenohumeral joint instability and is often difficult to diagnose in part because of a lack of knowledge about it (9). Athletes involved in overhead sports, such as tennis, are among those at highest risk (10). Few articles have specifically investigated posterior instability in elite athletes, with very little data on tennis players specifically.
Kinetic chain breakdown may result in increasing joint loads in distal segments leading to an increase risk of overuse injury. Weakness in the lower extremity, gluteal region, torso, and scapular stabilizers has been postulated to contribute to injury in overhead athletes, such as tennis players. In one tennis-specific study, it was demonstrated that not adequately flexing the knees in the cocking phase while serving resulted in a 17% increase in shoulder load and a 23% increase in elbow valgus load if resultant ball velocity was maintained at speeds comparable to those in players flexing the knees (11).
Static stabilization of the glenohumeral joint is collectively provided by the articular cartilage surfaces, glenoid labrum, capsular ligaments, and intraarticular pressure. Glenoid and/or humeral retroversion may contribute to posterior instability. Dynamic stabilization to posterior translation occurs primarily through subscapularis, with infraspinatus and teres minor strongly contributing at extreme ranges of motion. The main contributor toward posterior instability is the posterior capsulolabral complex. It is believed that posterior instability is initiated by insufficiency of the capsule, which secondarily leads to hyperlaxity of the joint (12).
Posterior instability in elite tennis player is thought to be caused by repetitive microtrauma to the posterior glenohumeral capsulolabral complex through chronic repetitive overhead stroke play, such as serving, especially the “kick serve” (hit with heavy top spin allowing for larger clearance over the net while still landing into the service box), which places large “peel back” forces over the posterior superior labrum and cuff (13,14). Additionally, evidence indicates players with reduced internal rotation, weak internal rotation isometric strength, and external/internal rotation strength deficits are at greater risk of developing a shoulder injury (15). Posterior instability most commonly presents as recurrent subluxation episodes, rarely if ever as a frank dislocation. Microtrauma to the posterior capsule, sustained during follow through, may allow posterior subluxation of the humeral head on the glenoid through the attenuation of the posterior inferior glenohumeral ligament (16).
Players will primarily complain of a general shoulder ache often anteriorly and weakness along the posterior joint line, or posterior superior aspect of the rotator cuff (16,17). They may have increased pain with certain positions or motions, such as cross-body adduction, serving, or smashing along with reduced power. They also may report numbness, paresthesia, weakness, or fatigue in the affected extremity. Symptoms intensify with the arm in 90° forward flexion, adduction, and internal rotation. Mechanical symptoms are uncommon (18).
Provocative measures, such as the Jerk, Kim, and circumduction tests, are useful in assessing for posterior instability and resulting pain, whereas load-and-shift testing can elucidate the extent of glenohumeral laxity. The Kim test has the highest sensitivity (80%) and specificity (94%) (19). The relocation test can be used to evaluate for internal impingement, or a “pinching” of the posterior superior cuff and labrum in abduction/external rotation position, and the sulcus sign suggests rotator interval capsular laxity. Although plain film imaging can be helpful in identifying any osseous abnormalities, for example, glenoid retroversion, magnetic resonance imaging (MRI) is the imaging study of choice for detecting posterior instability. Suggestive findings include posterior labral injury, posterior labro-capsular avulsion, posterior humeral head translation, avulsion or rupture of the posterior band of the inferior glenohumeral ligament, and a reverse Bankart lesion (17).
Conservative treatment is the initial intervention for posterior shoulder instability with a strong emphasis on deltoid and rotator cuff strengthening along with scapular and humeral head control (17). Strengthening the dynamic stabilizers of the glenohumeral joint, such as the rotator cuff and the periscapular musculature, may permit compensation for deficient static stabilizers, such as the labrum and the capsule. Attention to the kinetic chain looking for quadriceps tightness, gluteus medius insufficiency, and internal shoulder rotation deficits is emphasized along with a delayed reintroduction of the kick serve (1,15,20). A minimum of 12 wk rehabilitation is required to determine if conservative management will be successful (17).
Surgical treatment of posterior instability is indicated when conservative management fails to alleviate pain or prevent recurrent instability. Given that posterior capsule redundancy is the most common pathologic lesion tear, posterior capsular plication is recommended for patients with isolated unidirectional posterior instability without labral tearing (21). If a posterior labral tear is present, a posterior-inferior capsular shift is usually incorporated into the labral repair. In those cases of multidirectional posteroinferior shoulder instability, an inferior capsular shift toward the anterosuperior quadrant and closure of the rotator interval may be added to achieve stability (22).
Pathological Shoulder Complex (Impingement, Rotator Cuff Pathology, and Labral Injuries)
The serve motion produces high forces and large movements which place extreme demands over the shoulder, especially in the late cocking phase and early acceleration phase which has been established as the most harmful position for a tennis players shoulder, with the kick serve generating the highest forces (1,23,24). As a result of the demands placed on the shoulder in tennis, elite players develop mechanical adaptations in the dominant shoulder including reduced internal shoulder rotation, total arc motion, and increased external shoulder rotation (15).
Injuries to the shoulder account for 35% to 50% of all upper-extremity injuries, they are often overuse in nature, and are predominantly caused by overhead movements, such as the serve and “smash” (an overhead serve-like flat, straight shot hit with minimal spin) and have been associated with reduced isometric external rotation strength, imbalanced external/internal shoulder rotation ratio, and glenohumeral internal rotation deficits when compared with the nondominant shoulder (7,15,25). External rotation strength is important for decelerating the shoulder during follow through and providing stability. In fact, soft tissue imbalances have the ability to alter humeral kinematics resulting in impingement, rotator cuff pathology, and labral tears (15,23). These conditions can occur individually or as part of a pathological shoulder complex. This “internal impingement” occurs in the supraspinatus and infraspinatus tendons during the late cocking phase where contact between the greater tuberosity of the humeral head and posterosuperior glenoid rim leads to articular-sided fraying, partial and full thickness cuff tears, and SLAP tears (23,26,27). It is postulated that repeated contact and subsequent tissue damage occurs at a rate that exceeds tissue repair and/or torsional and sheer stress maybe responsible for rotator cuff and labral damage (23).
Players often report posterior shoulder pain usually in the late cocking phase and early acceleration phase; however, anterior shoulder pain can occur, as well as mechanical symptoms, such as instability and clicking (28). Pain is aggravated by serving and smashing with a subsequent loss of maximum power and later groundstrokes also may be impaired (28). Although clinical atrophy of the infraspinatus maybe present on examination, especially in higher ranked female players, it does not often appear to be associated with significantly compromised performance (29). Orthopedic examination should focus on investigating instability, rotator cuff pathology, impingement, and labral tears with tests, including anterior apprehension test, Jerk test, laxity (Sulcus sign), Full Supraspinatus Can, External rotation strength, Lift Off, Neer Test, Hawkins Sign, O'Briens Test, as well as the Burkhart et al. criteria for scapular dyskinesis (27–29). If intraarticular pathology is suspected, MRI is the principal imaging modality.
The cornerstone to treating the pathological shoulder complex should begin with conservative management, focusing on correcting the internal impingement potentiating factors. Scapular stabilization strengthening and stretching rehabilitation and injury prevention programs should focus on improving internal shoulder rotation range of motion, external shoulder rotation strength and restoring the external/internal shoulder rotation ratio, where external rotation strength is at least two thirds the strength of internal rotation (15,23,26,27). Great effort should be expended in reducing scapular protraction which may result from not only posterior capsular tightness, but pectoralis minor contracture. Reducing or removing serve loads, especially the kick serve may be appropriate early on with a graduate return to serve beginning with the slice serve, which has the lowest overall force and torque loads using a side spin to carry the ball toward or away from the receiver, reintroducing the kick serve last (1). Considerations also may be required to compact the serve motion by reducing the extremes ranges of motion during the late cocking phase (23).
Those players failing conservative management, arthroscopic surgery is indicated. Return to play following type II SLAP lesion repairs appears excellent at 93.9% in nonthrowing athletes. However, following rotator cuff repairs only 49.9% of professional athletes returned to the same level of play (30,31). Other procedures include posteroinferior capsulotomy to improve internal glenohumeral rotation and glenoidplasty (15,28).
Lateral elbow tendinopathy
Muscle tendon injuries are consistently the most common type of injury seen in elite tennis players, with overuse injuries more prevalent in the upper extremity. Lateral elbow tendinopathy (LET), formally lateral epicondylitis most often involves extensor carpi radialis brevis due to overuse of the wrist extensors or supinator (32). Postulated causes include excessive load, size of the racquet handle, weight of the racquet, poor technique, including a “leading elbow,” an open racquet face near the time of ball impact and contact in the lower half of the strings (32,33). Shock transmission has been proposed as a contributing factor in the development of LET, where those players with LET exhibit greater wrist extensor activity during ball impact and in early follow through (33). In addition to this, players with a double-handed backhand rarely develop lateral epicondylitis as the nondominant hand absorbs more of the energy (33). There is some evidence in recreational players that string tension also may be related to the onset of LET (34).
LET typically involves pain over the lateral elbow that often radiates into the forearm. Pain is bought on by resisted or loading the wrist extensors, there also may be a decrease in grip strength (32,33). Clinical tests include Cozen, Maudsley, Mills, and grip strength tests (32). Diagnostic imaging should not be routinely considered but may involve plain films and ultrasound, and MRI should be considered only for refractory cases. (33,35,36). As a tendinopathy, treatment needs to be multimodal focusing on removing and/or managing the excessive loads, correcting any technique faults and rehabilitating the tendon through mobilization and heavy load-based exercises (37–41). There is inconsistent data on the use of corticosteroid injections; at best, they appear to provide only short-term pain relief, whereas platelet-rich plasma (PRP) injections show better promise for intermediate and longer-term pain relief with lower risks of complications (42–44). Presently, there is no consistent evidence to support the use of extracorporeal shock wave therapy (45,46). Players failing conservative management after 6 months should be considered for surgery (35). For players using string shock dampeners, it appears that they do little to decrease the shock transmission to the forearm (47). An important differential diagnosis to be considered is entrapment of the posterior interosseous nerve.
Medial Elbow Tendinopathy
Wrist flexion is involved with all strokes, especially the serve and can result in overuse of the wrist flexor muscle group, primarily the pronator teres and flexor carpi radialis muscles (1,48). Traditionally, LET is reported more than medial elbow tendinopathy (MET); however, more recently, a ratio of 3:1 toward MET has been reported in the men's game most likely because of the predominance of the forehand and serve in the modern game (2). The clinical presentation is characterized by persistent medial elbow pain which is localized to the epicondyle but may refer into the forearm (49,50). Pain may be seen in the late cocking phase of the serve motion or during the early acceleration phase of the serve and/or forehand as the wrist snaps forward (2,49). There may be decreased grip strength, along with pain on resisted wrist flexion and pronation (49). As another overuse tendinopathy, the workup and treatment are similar to LET with plain films and ultrasound being the primary imaging modalities but are not usually required. Treatment focus is on removing the excessive loads, correcting any technique faults, and treating the tendon with heavy load-based exercises.
Elbow Medial Collateral Ligament Pain
Progressive elbow instability must be a consideration in the elite player with medial elbow pain. The medial collateral ligament (MCL), also commonly referred to as the ulnar collateral ligament (UCL), is placed under high valgus stress load in the late cocking and early acceleration phase of the serve motion between 20 degrees and 120 degrees of flexion, with evidence indicating these stress loads can be compounded by reduced internal shoulder rotation or scapular protraction (1,51). MCL injuries predominantly occur chronically from repetitive high valgus forces, rarely is the onset acute (52). At times, players will complain of a “pop” followed by medial elbow pain after a serve; more often, players will describe a history of recurrent medial elbow pain felt during the late cocking phase of the serve with subsequent loss of power and accuracy (53). A successful diagnosis can be ascertained from a thorough history and physical examination with MRI as the imaging modality of choice. Pertinent examinations should include the valgus stress test, milking maneuver, and moving valgus stress test (52,53). MCL instability is rated based on MRI findings: grade I — intact ligament with or without edema, grade IIA — partial tear, grade IIB — chronic healed injury, and grade III — complete tear (52,54). Workup also may include plain films to investigate for any fractures or ossification of the MCL. Dynamic ultrasound can be beneficial in demonstrating medial joint laxity and injury; however, MRI is the preferred choice of some providers for differentiating between partial and complete MCL tears (53,54).
Management of significant MCL injuries has traditionally involved surgical reconstruction with high return to play success rates of 80% to 94%; however, the recovery time is prolonged at 12 to 16 months (55). There is emerging evidence showing favorable outcomes for grades 1 and 2 injuries when PRP injections are combined with a rehabilitation program with success rates ranging from 88% to 91% with faster return to play ranging between 10 wk and 15 wk or quicker (54,56). For complete tears, surgery is required (57). Additional attention in the tennis athlete needs to be given to playing loads, the kinetic chain, including serve biomechanics, as well as investigating for any coexisting shoulder injuries or deficits resulting in MCL overload.
Distal Humeral Bone Stress
The incidence of bone stress injuries increased both in men and women at the Australian Open (2.1 and 2.4 times), and although bone stress injuries of the humerus are not common, they do occur in elite players and should be considered in players with mid to distal upper arm pain without a history of prior injury (58,59). Bone stress injuries are associated with excess work load — often match play and/or altered biomechanics, and in tennis is thought to be directly related to the serve motion (20,60). The proposed injury mechanism suggests that high stress loading of the humerus occurs during the acceleration phase of the serve because of the internal rotation and high valgus stress occurring at the elbow (20). It has been suggested that poor leg drive and/or coexisting injuries at the shoulder or elbow also may contribute to the increased loading of the humerus (20,60).
Symptoms and signs include increasing pain when serving which continues postmatch, arm fatigue, a history of either medial or lateral elbow tendinopathy, palpable pain over the distal humerus, commonly in the anterior and medial region and elbow hyper extension of 5° to 15°. Range of motion is usually full; however, pain may be noted at end ranges, a “humeral squeeze test” in two planes, medial to lateral and anterior to posterior may help to determine the exact location of pain (59). Plain films have low sensitivity for stress fractures, while MRI will reveal medullary edema +/− periosteal changes associated with early bone stress changes (20,60).
Early detection and intervention are the key for a quick return to play, with treatment focusing on relative rest, analgesics, and strengthening of the upper limb and trunk. 25-hydroxycholecalciferol vitamin D levels should be ascertained because deficiency may potentiate bone stress injury (61). Furthermore, analysis of the serve motion, paying particular attention to the leg drive phase to establish any technique deficiencies should be undertaken (20).
ECU tendinopathy and instability
Wrist injuries account for approximately 29% to 43% of all upper-limb injuries, occurring in both male and female players, although female players appear to exhibit a higher incidence (5,7,62). As the speed and power of the modern game increases, especially the top spin forehand, wrist positioning plays a vitally important role in generating higher racquet head speed (63). Grip position is, therefore, a key component of this, and evidence indicates a link between a player's grip (western and semiwestern) and wrist injury risk (63,64). Other risk factors include double-handed back hand (nondominant hand), increase use of the wrist to create top spin and higher string tension (62).
Grip type also determines the region of the wrist likely to be injured with western and semiwestern grips (Figs. 1 and 2) being associated with pain on the ulnar side because of increased loading in extension, ulnar deviation, and supination, while Eastern grips (Fig. 3) are linked with pain on the radial side (63,64). Wrist injuries on the ulnar side are more common than the radial side and include ECU tendinopathies, subluxations, ulnar collateral ligament enthesopathy, and triangle fibrocartilage injuries (63,65). Other documented wrist injuries with rare occurrence include ECU ruptures, ulnar bone stress in the nondominant wrist of players with a double-handed backhand, and hook of the hamate fractures (63,65).
Wrist injuries tend to be overuse-related, often involving repeated abutment of the hypothenar pad into the racquet handle in the case of hook of the hamate stress fractures or through repeated sudden movement from a supinated position into pronation resulting in stress forces over the ECU (63). Even acute traumatic wrist injuries like acute ECU ruptures or subluxation may potentially be due to chronic repeated microtrauma and failure of the local tissues.
The most common wrist injuries seen in tennis players are ECU tendinopathies and instability (62,64). ECU tendinopathies have a gradual onset, players often complain of pain early in the warm-up which improves as they play. Pain is located over the ulnar side of the wrist, there may be mild swelling over the ulnar sheath, and the ECU synergy test will cause pain (62,66). Ultrasound should confirm the tendinopathy, and as with any tendinopathy, treatment ought to focus on modifying or removing the excessive loads, modifying, or correcting any technique deficiencies, including grip position, mobilization, and heavy load-based exercises (37). If unresponsive to conservative management a corticosteroid injection into the fibro-osseous sheath should be considered along with short-term immobilization or splinting (66). Most players will continue to play through the injury with recovery taking anywhere from 2 wk to 24 wk (62).
ECU instability appears to be strongly related to players who use a double-handed backhand, with the wrist closest to the racquet head (62). Injury occurs due to tearing of the sheath of the sixth extensor compartment, it presents with intense pain with passive supination, pain over the ECU sheath, slight localized swelling, and a positive Cobra test (62,66). The onset can be acute and is often associated with a “snap,” “pop,” or chronic, the physical subluxation of the tendon from its natural groove only occurs with active contraction of the ECU (66). Dynamic ultrasound can, therefore, be utilized to reproduce the instability with MRI used to investigate the torn tendon sheath and surrounding structures (62,66).
ECU instability also can present without symptoms. Nonetheless, conservative management should be instituted early and involve wrist support. A corticosteroid injection may alleviate symptoms and result in a faster return to play (66,67). In those cases that fail to resolve with conservative management, treatment involves a plaster cast for 2 to 3 months with the wrist extended to 15°, with a possible follow-up MRI or ultrasound testing to ensure that the ECU is healing. Stress tests should be performed after 2 months of immobilization to check the stability of the ECU tendon. If instability continues, the cast should remain for a further 4 wks before retesting (62). Once the tendon is stable, return to play can occur after an additional 4 wks. Reconstructive surgery should be considered with chronic ECU instability or when the periosteum and tendon sheath strip off the distal ulnar and the tendon subluxes within an expanded subsheath. Return to play following reconstructive surgery may take up to 17 months (66). ECU ruptures are uncommon; however, two reported cases occurred after two or more corticosteroid injections (62).
Wrist Ulnar Collateral Ligament Injuries
Ulnar sided wrist pain in the nondominant wrist is increasingly observed in elite tennis players, with 17 players between 2011 and 2016 at the Australian Open seeking medical treatment for pain in the nondominant wrist (5,68). Although ECU pathology is likely to be the most common cause of ulnar-sided wrist pain in the dominant wrist in elite players (62,64,69), it has been reported in the nondominant wrist of players who use a double-handed back hand, with the potential cause thought to be linked to the eccentric contraction of the ECU muscle at the time of ball impact (69).
UCL abnormalities in the nondominant wrist of elite players have been reported to be twice as common in players with symptomatic wrist pain compared with players with asymptomatic wrist pain, giving rise to its potential involvement in ulnar sided wrist pain (68). UCL injuries can coexist with ECU pathology although they are often overlooked, especially in players who are purported to have ulnar styloid impingement. Consideration, therefore, should be given to a UCL injury in elite players who present clinically with maximal pain over the ulnar styloid compared with the asymptomatic side and MRI findings indicating UCL abnormalities in the absence of any other findings, with consideration that the relationship between clinical presentation and MRI abnormalities is not always clear (68).
Although there is little research currently available on UCL injuries in the nondominant wrist of elite tennis players, it is considered to be an enthesopathy of the UCL attachment to the ulnar styloid caused by both wrist compression forces during ulnar deviation in the double-handed back hand preparation phase followed by traction forces as the wrist rapidly moves into radial deviation. Grip and possible hand spacing also may be contributing factors (68). With a paucity of information available to guide treatment, a corticosteroid injection can often relieve the pain quickly, allowing for a graduated return to play within a couple of weeks.
The tennis epidemiology consensus statement has established a framework for studying and understanding more fully injury exposure rates and trends within elite tennis. However, there are still inconsistencies in how injury frequency rates are defined, as well as how injuries are reported. As a result, pooling injury data is difficult and may result in either overreporting or underreporting of injuries.
Previous reviews of upper-limb injuries in tennis players have been undertaken utilizing data which included a composite of recreational and competitive players (27,70,71). This review solely utilized injury reporting from the ATP, WTA, Davis Cup, and 3 Open Championship tournaments focusing on elite players. The common injuries of the upper limb remain consistent across all reviews: pathological shoulder complex, elbow tendinopathies, ECU tendinopathy, and subluxations. However, our review notes less common injuries seen in elite players that are of clinical importance: posterior shoulder instability, distal humeral bone stress, MCL pain in the elbow, and wrist ulnar collateral injuries in the nondominant wrist. To our knowledge, only distal humeral bone stress injuries in tennis players have been reported in the literature. Although there is a paucity of literature on MCL elbow pain in tennis players, the authors decided to include this because it is well documented in the Australian Open and Tennis Australia injury databases, and further investigation and research is warranted.
As has been reported in previous tennis epidemiology studies and is evident by the nature of injuries reported on in this review, a significant number of injuries in elite tennis players are overuse in nature. There is evidence to suggest that some of the acute injuries may be due to poor rehabilitation and/or a too early return to play especially in the case of muscle strains. This suggests that players and coaches are perhaps not managing soft tissue loads appropriately and are focused solely on peak performance. A compromise of training and rest will lead to suboptimal recovery and performance (72,73). Players and coaches need to be more mindful of ensuring recovery periods and making sure a player is fit to return to play. There indeed is a role for injury prevention programs in elite tennis to reduce the current injury rates, with evidence indicating warm-up programs, strength training, and multi-intervention training programs with a balance board reduce the risk of injury, while more specific muscle strain prevention programs reduce the risk of reinjury (74–76). While the Pas et al. (77) unsupervised e-health tennis injury prevention program in recreational tennis players did not reduce the risks of tennis injuries, further research is required to investigate the efficacy of a supervised injury prevention program in elite players.
The authors declare no conflicts of interest and do not have any financial disclosures.
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