Shoulder pain affects up to 67% of the population at some point in one's lifespan (46). Common diagnoses implicated in the etiology of shoulder pain include, but are not limited to, impingement syndromes (e.g., subacromial, subcoracoid, and internal), osteoarthrosis, labral tears, and soft tissue pathologies of the rotator cuff, such as tendinopathy (8). Of the various diagnoses attributed to shoulder pain, it has been estimated that approximately 65% of individuals present with some form of rotator cuff pathology (e.g., tendinopathy and tear), with the supraspinatus and infraspinatus most often affected (8).
Tendinopathy is a collective term used to describe pathology within, and pain arising from, the tendon itself. A considerable shift has taken place within the sports medicine professions regarding the understanding of tendon pathology, the terminology used to describe such pathology, as well as management strategies. This article presents a current discussion of the continuum of tendinopathy classification, an overview of risk factors and more common patient or client symptoms, as well as evidence underpinning common pharmacological and exercise-based interventions. The focus of the discussion will be on the supraspinatus and infraspinatus tendons, hereafter referred to as the rotator cuff tendon.
ROTATOR CUFF TENDON ANATOMY
Although a comprehensive discussion of tendon anatomy and physiology are beyond the scope of the article, a brief overview is necessary to understand the content presented in latter sections. Tendons are soft tissue structures interposed between a muscle and bone and allow for transmission of forces from the muscle to the bone, resulting in movement (33). The term myotendinous junction describes the area where tendon unites with the muscle, whereas the tenoperiosteal region is where the tendon connects to bone (44). Regarding the shoulder, evidence from anatomical studies has shown that the supraspinatus and infraspinatus tendons fuse near their insertional point forming a conjoined tendon (15), which clinically lends to grouping the 2 muscles together regarding diagnosis and management strategies.
The supraspinatus tendon, in addition to the conjoined insertional point it shares with the infraspinatus, blends in with other soft tissue structures such as the coracohumeral ligament and rotator interval (15). Recognizing these blended insertional points help to explain why a specific diagnosis of supraspinatus tendinopathy alone may be challenging from a clinical perspective (e.g., patient has pain with resisted external rotation as well as abduction). From a composition perspective, tendons are generally composed of a dry mass (collagen, elastin, and cells) and water (44). The basic components of a tendon (Figure 1) include bundles of collagen (which are inclusive of collagen fibers and smaller subunits referred to as fibrils) (45), tenocytes (the cells of the tendon), and ground substance (proteoglycans, glycosaminoglycans, and other small molecules) (33,44). Approximately 65–85% of the collagen in a healthy tendon is type 1 (has tensile strength) with weaker type 3 collagen presenting in trace amounts (44,45). Interestingly, evidence suggests a greater proportion of type 3 collagen in degenerative supraspinatus tendons (44,60).
Proteoglycans, which are part of the ground substance, attract water, provide structural support for the tendon, and regulate the process of maintaining an extracellular matrix. The term extracellular matrix is often used in the literature to collectively describe the structures within a tendon including collagen fibers, proteoglycans, and connective tissue sheaths that surround the various tendon bundles (epitenon, paratenon, and endotenon) (33). The ground substance of the extracellular matrix provides structural support for the collagen fibers (44). These anatomical terms are relatively important to understand because pathological changes often refer to degradation of the extracellular matrix and favorable responses to loading (exercise) often involve communication to the tenocyte, which influences the collagen composition.
The tenocyte is the primary cell found in a tendon and is anchored to the collagen fibril (44). These cells (multiple in each tendon) are of particular importance because they form a load-responsive signaling network that allows them (the tenocytes) to communicate with each other (34). Tenocytes are responsible for maintaining the extracellular matrix in response to changes in loading, growth, and repair (45). Essentially, tenocytes sense changes in loading and produce a cascade of physiological responses (34). A key response is to stimulate collagen (protein) synthesis when subject to appropriate mechanical load (e.g., resistance training). It is important to recognize that each tenocyte has an outer cellular membrane, a nucleus containing the cell's DNA, which resides in a cytoplasm, and integrins (proteins) that provide a means of communication between the tenocyte and extracellular matrix (34). Essentially, integrins communicate mechanical loading and signals from the extracellular matrix across the cellular membrane to the tendon cell (34). Evidence suggests that with degeneration or injury, tenocytes decrease in number and contribute more toward the development of type 3 collagen (44).
Tendons are susceptible to both normal and abnormal loading (18,44). Although tendons are designed to withstand mechanical forces and appropriate loading produces favorable adaptation, loading deemed excessive or beyond the “developed” capacity of the individual tendon may lead to pathology (18). Physical environments responsible for abnormal loading include those that produce tensile strain, compression, and shearing. In addition, pathological changes may occur from inadequate loading, which has been referred to as stress shielding (59). Unfortunately, there are no defined criteria for aberrant versus normal loading because each tendon and person is unique. An understanding of risk factors (presented in a subsequent section) may assist the sports medicine professional in recognizing those circumstances (e.g., age, medications, etc.) or individuals who may be prone to aberrant loading.
Regarding tensile forces, repeated or unaccustomed end-range strain can lead to ischemia and microtrauma, such as fibril tearing, as well as damage to the extracellular matrix and tendon cells (60). Moreover, unaccustomed loading that is either rapid or repeated may lead to tensile strain despite being within the tendon's physiological range. Compression loading would occur in conditions where the tendon wraps around a bone and in narrow areas such as the subacromial space (seen in subacromial impingement syndrome) (60). Excessive compression leads to abnormal changes in the tenocyte (stiffer cartilage-like matrix) characteristic of tendinopathy. In addition, areas of tendon compression (as it wraps around a bone) are often associated with reduced blood flow, and subsequently are a common site of tendinopathy (45). Finally, shearing occurs at points of friction as the tendons interface with other soft tissues or between the tendon's fascicles (bundles). For example, the supraspinatus tendon is known to produce shearing within the fascicles, and as a result, proteoglycans may be found between such fascicles to minimize aberrant shearing forces. Nevertheless, partial tearing of the supraspinatus may be the result of shearing as described, compression as the tendon wraps around the humeral head (increased during adduction) or impingement at the subacromial space (which would be seen with subacromial impingement syndrome), or tensile forces from nonphysiological forces (e.g., trauma), or overzealous stretching (60).
On a more positive note, appropriate loading of a tendon produces a favorable response referred to as mechanotransduction (34). Mechanotransduction is the process whereby a mechanical effort or load (e.g., resistance training with appropriate overload) leads to a cellular response in the tissue being loaded. These cellular responses may produce a structural change in the tendon architecture. Similar to bone getting stronger in response to weight bearing (another form of mechanotransduction), tendon would remodel in response to loading. Mechanotransduction follows a sequence of 3 steps, which includes mechanocoupling, cell-to-cell communication (passing of loading message from one area of tendon to another), and a cellular response such as collagen synthesis (34).
A prerequisite for mechanotransduction is an appropriate load to the tissue of interest. The physical load that induces mechanotransduction is referred to as mechanocoupling (34). A key point with mechanocoupling is that the “overload” needs to be appropriate, progressive, and not to a point where injury might be the outcome. For example, eccentrically overloading (mechanocoupling) the involved tendon sets off the remaining physical events of mechanotransduction through stimulation of the tendon cell (tenocyte), which in turn leads to cell-to-cell communication and a cellular response (collagen synthesis).
Although the aforementioned example references a single cell, the loading response would affect numerous cells through communication channels unique to tendon. In other words, when one tendon cell is stimulated through mechanocoupling (shear, compression, and tensile), the signal is received at distant cells not subject to the load (34). This is a critical point and works in favor of adaptation. This process occurs through the signaling proteins inositol triphosphate and calcium within the tendon (34). For example, assume that the supraspinatus and infraspinatus conjoined tendon is subjected to an eccentric overload. The physical load (mechanocoupling) is registered at the tendon cells under stress. Tendon cells have an inner connecting network that communicates with each other through areas referred to as gap junctions. Signaling proteins, as previously described, communicate the load through gap junctions to other cells of the supraspinatus and infraspinatus tendon. The ultimate goal of applying a physical load is the cellular response that, in the ideal environment, promotes tissue repair and remodeling through collagen synthesis. A detailed discussion of mechanotransduction with illustrations of the cellular processes described can be found in the article by Khan and Scott (34).
In summary, for mechanotransduction to occur, a load is applied to the tendon extracellular matrix. This load, through integrins, communicates the load's message to the tendon cell where the DNA is located. When the signal of a “load” is received at the tendon cell, a message is communicated to the cell's nucleus (DNA). Once the nucleus receives the signal, the messenger RNA transcribes the message and shuttles it to the cytoplasm where it is likely translated into collagen synthesis. This collagen is ultimately incorporated into the extracellular matrix. Fortunately, the mechanical load on the tendon induces other positive anabolic responses that further support remodeling of the extracellular matrix. For example, eccentric overload activity has been shown to induce autocrine and paracrine insulin-like growth factor (anabolic hormone) responses in the tendon and muscle (29), which further supports and influences matrix remodeling.
PATHOPHYSIOLOGY AND CLASSIFICATION
The pathogenesis of rotator cuff tendinopathy is multifactorial with both extrinsic (subacromial impingement) and intrinsic changes (e.g., degeneration) occurring within the tendon. Irrespective of the pathogenesis, tendon pathology generally encompass the spectrum ranging from acute trauma with a direct tear to microtraumatic (abnormal loading response) changes that, over time, follow a pathological continuum (18). In short, microtraumatic changes, in the absence of healing, may progress to tendon degeneration and potential rupture. Although traumatic tears are relevant, the focus of this section will be on the continuum of tendon pathology ranging from early reversible changes to irreversible degenerative changes and potential rupture. Because of the complexity of tendon pathology, this section will focus on noncalcific tendinopathy.
The sports medicine profession has evolved dramatically in the last decade regarding the understanding of tendon pathology. Current nomenclature has abandoned the umbrella term tendinitis in favor of the term tendinopathy (18,47,60). In short, tendinopathy represents a nonrupture tendon injury that, over time, may lead to partial or complete tearing. Much of this shift has evolved from studies that suggest an absence of inflammation, in most, but not all clinical cases of tendon pain (18). Moreover, in cases where inflammatory cells are identified, it is a nontraditional response (19). From a stage-based perspective, tendon pathology may be subgrouped into 3 main phases (Table), which include the reactive stage (e.g., reactive tendinopathy), tendon disrepair, and finally, degenerative tendinopathy (e.g., tendinosis).
Reactive tendinopathy is a response that occurs from acute overload or microtrauma (1). In this stage, inflammatory cytokines may be present (40) because of the need for matrix synthesis and degradation. Proliferation occurs, which includes an increase in proteoglycans, which attract water and promote subsequent changes to the tendon matrix (18). This results in an appearance of a thickened tendon (18). The thickening may serve to reduce further stress or allow for some degree of adaptation; however, this must be recognized as a different response than what would be expected from normal progressive loading. Normal progressive loading would result in a stiffening response with insignificant thickening. In the reactive stage, there is no tearing of the collagen fibers. It is important to recognize that thickening of a tendon may induce pathology in areas where space is limited such as the subacromial region, leading to subacromial impingement (40), which explains why rotator cuff tendinopathy and subacromial impingement concurrently exist in many cases (8). One should recognize that tendons require overload to adapt; however, it is the rate and duration of loading that would lead to a reactive response as described. Once again, the challenge here is recognizing that there is little information on what might be a cut point between normal (e.g., optimal) loading that would induce an adaptation versus that which would lead to reactive tendinopathy. A key point to consider, in cases where a potentially abnormal load occurs, is adequate load management (reduction of abnormal loading). Moreover, evidence suggests that in most cases, this stage is not associated with inflammation of the tendon per se (18); rather, inflammatory changes of the subacromial bursa are likely to be present (40).
Tendon disrepair is the next phase in the continuum of pathology whereby the tendon may have attempted to heal; however, there is greater degradation of the extracellular matrix (18). Inadequate rest (i.e., reduction of microtrauma) or a failure to adequately load the tendon (e.g., stress shielding) may influence the progression of reactive tendinopathy to disrepair (59).
Tendon disrepair is associated with an increase in chondrocytes and fibroblasts resulting in a more pronounced increase in proteoglycan production (18). The increase in proteoglycans leads to further disorganization of the matrix and displacement of collagen fibers, which alters the loading capacity of the tendon (18). Moreover, there may be evidence of neovascularity (new blood vessels) and neuronal (nerve) ingrowth; however, neovascularization is not clearly present in the supraspinatus when compared with other regions of the body (e.g., Achilles tendon) (18,40). The potential for reversible changes at this stage remains; however, further insult to the tendon may lead to irreversible degenerative changes and potential rupture.
Degenerative tendinopathy is the final stage in the continuum of tendon pathology (18,40). This phase is characterized by a failure to heal and further unfavorable changes to the tendon matrix (degradation), which include cell (tenocyte) death (18). Areas of cell death will exist and further degradation of the matrix includes potential neovascularization and ingrowth of nerves (18). It is important to recognize that although neovascularization and neuronal ingrowth are indeed part of the tendon pathology sequela, the evidence for the presence of it at the supraspinatus is less convincing than at other areas such as the Achilles tendon. Moreover, there are fibroblast type cells in the tendon, which can undergo metaplasia to form tissue such as adipose and cartilage, explaining why these tissues are found in degenerative tendons. At this stage, there is little potential for natural reversal. In most of the ruptured tendons, degenerative changes are present. The supraspinatus is unique when compared with other regions of the body because it undergoes a thinning process (49) at this stage, which is additionally associated with tearing.
In summary, tendinopathy may be viewed as a continuum ranging from early reactive changes which, in the absence of appropriate loading and perpetual microtrauma, leads to degeneration and potential tearing. Architectural changes in the tendon resulting from pathology include a disorganization of collagen fibers, potential neovascularization and neuronal infiltration, increased water content in extracellular matrix, type 3 collagen that is poorly organized, tissue breakdown and tearing, as well as areas of cell death. One should recognize that although a particular patient may be in the degenerative (tendinosis) stage, an element of reactive tendinopathy might be present with additional events of abnormal loading. On a positive note, adequate rest and removal of microtrauma would allow the tendon time to respond and improve the tendon's capacity to endure further loading without injury (40). It is important to recognize the need to resume progressive loading at the appropriate time because an absence of loading or failure to load may accelerate or induce the continuum of tendon pathology through stress shielding.
RISK FACTORS: ROTATOR CUFF TENDINOPATHY
As stated in the previous section, the etiology of tendinopathy is multifactorial with both extrinsic and intrinsic risk factors. Extrinsic risk factors generally involve some type of impingement syndrome directly compressing the tendon. With respect to the supraspinatus and infraspinatus, subacromial impingement syndrome is most common (44). Intrinsic risk factors are those that occur within the tendon itself and present the focus of this section.
Risk factors for rotator cuff tendinopathy include, but are not limited to, age, overuse, obesity, smoking, diabetes mellitus, and medications (e.g., fluoroquinolone antibiotics, statins, and glucocorticoid corticosteroids). Obesity and higher body mass index levels (>25) have been associated with both shoulder and elbow tendinopathy (25,66). Additional risk factors for tendinopathy include smoking (2 times more likely than a nonsmoker) as well as repetitive and forceful overuse activities (56). The strongest intrinsic risk factor for shoulder tendinopathy is advancing age (67). Evidence suggests an overall lifetime prevalence of 9.7% in patients aged 20 years and younger to upward of 80% in those in their 80s (62). Moreover, the point prevalence (cases at any one given point) has ranged from 2.4 to 14% among individuals less than 70 years of age and increases to 21% when analyzed without age exclusions (43).
Certain medications have been associated with tendinopathy and rupture. Statins, for example, are used to treat hypercholesterolemia; however, a body of evidence does suggest a risk of tendinopathy. Fortunately, most of the reported incidents resolve with discontinuation of the medication. Although epidemiological data are limited, evidence suggests that 2% of those on statins will experience tendinopathy from the medication with men more likely than women (22). Other medications associated with tendinopathy include the fluoroquinolones (Ciprofloxacin [Cipro], Levofloxacin [Levaquin], and Moxifloxacin [Avelox]) and corticosteroids. Fluoroquinolone users have a 1.7-times greater risk of tendon disorders than someone who is not taking this drug. Interestingly, the risk increases to 3.1-times if taking it concurrently with an oral corticosteroid (20). Thus, it is seemingly important to recognize the risk of concomitant administration of drugs that may potentiate tendinopathy (22). The effects of corticosteroids are discussed in subsequent sections. A key point regarding medication use is the nature of concurrent physical interventions. Sports medicine professionals who are working with individuals taking one of the medications associated with tendinopathy should be cautious and avoid overzealous advancements in favor of a gradual progression of loading.
The diagnosis of rotator cuff tendinopathy should be determined by a qualified medical professional, which may include various members of the sports medicine profession. With this being stated, determining a diagnosis of rotator cuff tendinopathy is well beyond the scope of this article. Nevertheless, a general understanding of the physical presentation is important to appreciate the management strategies discussed in latter sections and potentially identify a client needing to be referred to a qualified medical professional.
The diagnosis of symptomatic tendinopathy is primarily clinical with imaging often useful for confirming a structural etiology (60). Unfortunately, imaging is not always a good indicator of clinical symptoms because asymptomatic individuals may present with abnormal findings on magnetic resonance imaging and diagnostic ultrasound. Thus, patients or clients may mention imaging-related pathology that may not necessarily coincide with their presentation or abilities.
Tendinopathies are generally characterized by activity-related pain, localized tenderness, pain with resisted muscle contraction, and limited mobility (32,60). Rotator cuff tendinopathy of the supraspinatus and infraspinatus often coexists with subacromial impingement syndrome, which is considered an extrinsic risk factor for tendinopathy. The symptom presentation would be consistent with pain present at the anterolateral shoulder (primarily at the anterior and lateral deltoid regions) rarely crossing the elbow (6). Discomfort would be activity related (particularly when reaching overhead owing to an association with subacromial impingement) and worsen at night when sleeping on the affected side (41,54). Muscle activation of the supraspinatus (abduction [lateral deltoid-raise position] or empty-can position) (36) and infraspinatus (external rotation) would produce pain and, potentially, weakness depending on the stage and presence of tendon disrepair or tearing (54). Evidence suggests that the empty or full-can positions are optimal for testing the supraspinatus and infraspinatus; however, it is difficult to isolate a contraction specific to these tendons because deltoid muscles are active during these tests (36). Evidence suggests that individuals with subacromial impingement syndrome often report pain with lateral deltoid raises and upright rows when the elbows upwardly advanced beyond shoulder height (37). Palpation at the insertional points of the supraspinatus and infraspinatus tendon would likely identify pain and focal tenderness as well (64). In addition, evidence suggests that nearly half of people with rotator cuff tendinopathy have a reduction in the subacromial space when elevating the arm overhead (58), which may impinge the rotator cuff tendons; thus, as previously stated, subacromial impingement is a coexisting diagnosis and explains similarities among individuals with tendinopathy (54).
The conservative management of rotator cuff tendinopathy includes interventions believed to alleviate symptoms, corrective exercises that may have an impact on tendon structure, and supportive measures designed to mitigate recurrence and risk factors. More common conservative interventions include, but are not limited to, pharmacological and exercise-based therapies (3,4,9,42). A brief evidence-based discussion of the aforementioned management strategies is presented to provide the sports medicine professional with the information necessary to understand the utility of these interventions and potential risk profile where appropriate.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used for the treatment of tendinopathy (7). NSAIDs inhibit the cyclooxygenase enzymes (COX-1 and COX-2), which subsequently inhibit production of prostaglandins and thromboxanes, the instigators of pain and inflammation (14). These medications include but are not limited to Ibuprofen (Motrin and Advil) and Naproxen (Aleve and Naprosyn). Selective NSAIDs that specifically target COX-2 impede the production of inflammatory prostaglandins while sparing the beneficial effects that the COX-1 enzyme has on normal physiological cell function. Because of their selectivity, COX-2 inhibitors such as Meloxicam (Mobic) and Celecoxib (Celebrex) have a lower incidence of gastric irritation (61).
NSAIDs can affect tissue histology, physiological function, and mechanics, as well as the individual's subjective reports and gross movement. Evidence on the efficacy of their use for shoulder tendinopathy is minimal, and that which is available has been contradictory (3,7). A reduction in edema and the accumulation of inflammatory cells within the paratenon (Figure 1 for tendon anatomy) has been shown, proposing that NSAIDs may be of some value during the “inflammatory” or reactive stage of tendinopathy (48). Although short-term (<2 weeks) use of NSAIDs has not demonstrated a deleterious effect on healing within the tendon, evidence has suggested that tendon-to-bone healing after tendon repair surgery (including supraspinatus) may be impaired by poor collagen organization and maturation (13), decreased tenocyte migration and growth, and decreased tensile strength with the utilization of NSAIDs (16,65). Both selective and nonselective NSAIDs have been associated with a significant decrease in failure load (reduced tolerance to load), increased incidence of postoperative repair failure, and decrease in collagen content in animal tendon repair sites (24). These findings suggest that NSAID use may be deleterious during postoperative care; however, the degree that an animal study can be generalized is not clear. On a more positive note, 4 weeks of NSAID use has resulted in reduced shoulder pain and improved shoulder abduction range of motion in comparison with a placebo (7). These findings complicate decision making because the individual may report improvement in pain and function, whereas microscopic effects on tissue quality may be negative.
Corticosteroid injections (CSIs) aimed at targeting the rotator cuff are directed to the subacromial region. Research on the efficacy of subacromial CSI has produced variable results (4,50). Age, sex, arm dominance, duration of symptoms, presence of a full-thickness tear, baseline activity level, or severity of symptoms have not been shown to affect outcomes in individuals who receive CSI (17). Individuals with rotator cuff tendinopathy, who underwent CSI, have demonstrated improvement in pain, abduction and internal rotation range of motion, as well as functional abilities as early as 1 week and up to 6 weeks after treatment (31). Unfortunately, evidence has shown that improvements are often transient and no significant difference in range of motion or pain levels exist after 12 weeks (50). In comparison to oral NSAID use, CSI produced a greater reduction in pain, especially in the short term (4,27) and a CSI has resulted in a greater reduction in pain at night, at rest, and during movement than other treatments (23).
Most of the studies investigating the histological changes that occur with CSI have focused on the Achilles and patellar tendons and have demonstrated a loss of collagen organization, increase in collagen necrosis, decreased growth and viability of fibroblasts, and increased cellular toxicity. Mechanical changes in tensile strength and increased elastic stiffness have also been found (21). A single-dose injection has demonstrated adverse effects on collagen formation in the extracellular matrix and inflammatory cytokines in the infraspinatus tendons of rats (38). Five CSIs into the shoulders of rats have resulted in increased inflammatory cells such as macrophages and giant cells within the collagen bundles and clear signs of necrosis and fragmentation of collagen bundles. These changes were not present in those animals that had only received 3 injections, suggesting that injections should be used in limited quantity (63). Furthermore, both CSI and NSAIDs have been shown to affect fibroblast differentiation into tenocytes with proliferation of adipocytes (26), which may increase the possibility of macrotrauma (ruptures) to the tendons. These findings may indicate limited efficacy of a CSI during the disrepair and degenerative stages of tendinopathy. Moreover, sports medicine professionals should be cautious when working with clients who have had numerous CSIs because the potential for injury is seemingly increased.
Exercise-based interventions have consistently performed well in the literature for rotator cuff tendinopathy as a means for reducing pain and improving function (42,43). Although a superiority of one approach versus the other has not been consistently established in well-designed studies, evidence supports the use of eccentric overload training among various subgroups including individuals who have been recalcitrant to general exercises and interventions (9,10,12,28,51).
Eccentric exercise has become a well-researched topic in recent years, with implications for the rehabilitation of a multitude of conditions. Eccentric exercise involves the production of force as a muscle is lengthened, which facilitates deceleration (9). A muscle and tendon can withstand a greater load during an eccentric action when compared with a concentric contraction. Thus, exercise routines for the shoulder designed to produce eccentric overload often involve use of a load that may not be feasible with a traditional exercise. For example, standing eccentric elastic band external rotation would require the use of a band resistance that is generally too heavy for traditional (repetitive) concentric external rotation. The eccentric overload would be accomplished by using the opposite arm to assist with the concentric phase followed by a slow eccentric return to the initial position (Figure 2A–D, See Video, Supplemental Digital Content 1, https://links.lww.com/SCJ/A222) (10–12). Thus, the eccentric phase is adequately loaded in the aforementioned example as the contralateral arm is needed for the concentric phase. These factors theoretically help promote tissue remodeling by affecting the histological changes that occur with tendon pathology (9,57). Eccentric exercise has been postulated to cause a localized decrease in tendon thickness, normalize the tendon structure (53), and break down neovascularization that may be a source of pain (52). A more detailed discussion of the effects of eccentric training for shoulder disorders may be found in previously published columns in Strength and Conditioning Journal (10,11).
Evidence on the efficacy of eccentric training for rotator cuff tendinopathy is limited when compared with other conditions such as Achilles tendinopathy, patellar tendinopathy, and lateral epicondylalgia (51). Histological changes in supraspinatus tendinopathy are similar in some ways to the changes noted in the Achilles tendon; therefore, research findings that advocate eccentric training for Achilles tendinopathy have been cautiously applied to shoulder pathology (9). A recent randomized controlled trial found superior efficacy for pain and function among individuals with subacromial pain syndrome (and associated clinically diagnosed tendinopathy) who were exposed to a daily eccentric overload program for the shoulder external rotators (12). In the aforementioned study, the authors performed eccentric only for the external rotators and excluded specific eccentric overloading exercises that required overhead movements, which may have led to improvements in pain that were superior to previous studies (9,12). Moreover, eccentric rotator cuff strengthening has been efficacious for reducing pain and improving function among individuals with subacromial impingement and rotator cuff tendinopathies scheduled for surgery, ultimately leading to cancellation of surgery for many subjects (5,28).
The most appropriate dosage for eccentric training is yet to be determined (51); however, the protocol that is most often followed was developed by Alfredson et al. for the Achilles tendon. Exercises, using the Alfredson protocol, are performed for 3 sets of 15 repetitions, twice daily, 7 days per week, for 12 weeks. This protocol has resulted in increased peak torque, decreased pain, and a return to previous level of function (2). Clinical outcomes are not affected by location of exercise performance (clinic-based versus home-based) or pain during exercise (provocation versus avoidance) (43). A recent investigation found that performance of such exercises once daily may offer similar benefits to twice daily for individuals with shoulder conditions known to be associated with tendinopathy (12). Despite the aforementioned evidence, the decision to incorporate an exercise or specific dosing strategy involves numerous considerations that are inclusive of the patient or client presentation above all (35).
An alternative to eccentric overload training that may be of value during the early stages of symptomatic tendinopathy or in preparation for more advanced loading strategies is isometric strengthening. Although the research on isometric training is limited, evidence does suggest a beneficial response for acute tendinopathy (55). In particular, evidence from an investigation (3-arm [group] trial) has indicated that isometric strengthening produced significant improvements in pain and function as well as reduced tendon thickening (observed for 71% of participants albeit not statistically significant) after intervention (55). Unfortunately, the details of the isometric dosing were unclear because the authors reported progressing from 3 to 5 times per day with the duration of contraction progressing from 10 to 20 seconds with no mention of repetitions performed with each session. Moreover, only 13 subjects with acute rotator cuff tendinopathy were used, and the intervention was limited to 1-week suggesting that the results cannot be generalized for those who are not in the acute stage.
Although a paucity of research exists for isometric strengthening for rotator cuff tendinopathy, additional evidence may be gleaned from studies of isometric training for other regions of the body. For example, one study of older adults evaluated pain perception and pressure pain thresholds in response to isometric training of the elbow flexors at various intensities and durations of isometric contraction (39). Specifically, the study evaluated 3 dosing protocols which included: 3 full-effort brief maximum voluntary isometric contractions (MVICs), 25% MVIC held for 2 minutes, and 25% MVIC held until unable to maintain force. The MVIC was determined through the use of a force plate and pressure pain thresholds determined at the finger. After the isometric efforts, improved pressure pain thresholds and reduced pain (analgesia) were found across all intensities and durations (39).
Another study evaluated the dose response of isometric elbow flexion contractions on pain perception (e.g., pressure pain thresholds and pain rating) in healthy adults aged 18–42 (30). Specifically, dosing included 3 brief maximum-effort MVICs, 25% MVIC held for 2 minutes, 80% MVIC until unable to maintain force (failure), and 25%, and held until unable to maintain force (failure). Results of the study indicated that improvements in pressure pain thresholds occurred after the 25 and 80% MVIC held until failure dosing as well as the brief full-effort MVIC dosing. The 25% MVIC for 2 minutes did not significantly change the pressure pain threshold. Regarding pain rating, the 25% MVIC held until failure had the greatest reduction in pain rating as well.
In summary, an evidence-informed interpretation of the literature suggests consistent findings with respect to isometric contractions offering an analgesic effect. From a dosing perspective, there are no specific guidelines for isometric prescription; however, daily performance of either maximum effort (brief or until failure) or low intensity until failure dosing seems to be appropriate. It would seem reasonable to prescribe isometric strengthening exercises for tendinopathy in the acute stages with ultimate progression to eccentric overload training for the long term. Among those individuals who are not considered “acute” and who are not accustomed to overload training in general, isometrics may serve a useful beginning point for targeted loading of the rotator cuff tendons. Performance of isometric loading may be performed as illustrated in Figure 3.
Tendinopathies have evolved over the past few decades from an inflammatory “tendonitis” thought process to a greater understanding of the continuum of pathology, which essentially is a failed healing process associated with inappropriate or inadequate loading. Upper-extremity tendinopathies have a multifactorial etiology; thus, one's individual risk should be evaluated when designing exercise programs (35). Prevention resides in the attenuation of risk factors, whereas evidence seemingly suggests a short-term benefit from anti-inflammatory medications, as well as a benefit from both isometric and eccentric exercise when combined with a global exercise program. Although a structural change (reversibility of tendinopathy) in response to eccentric training has not been identified at the rotator cuff, evidence favors utilization for other benefits. Specifically, isometric and eccentric overload training of the shoulder external rotator musculature offers a favorable benefit with respect to reducing pain, increased strength, and improved function. Thus, it seems reasonable to incorporate eccentric training into exercise programming for individuals with rotator cuff tendinopathy.
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