Partial and full tears in supraspinatus tendons, a rotator cuff tendon. (a) The location of the supraspinatus tendon. (b–d) X‐ray images of a partial‐thickness tear in the supraspinatus tendon. In a neutral position (b), a partial tear was not evident; hence, changes were interpreted as tendinosis. Crass position (c) and modified Crass position (d) show a hypoechoic region (arrows) interpreted as a partial tear in a fat‐suppressed T2‐weighted magnetic resonance image. (e and f) Full‐thickness tear (arrows) of a supraspinatus tendon (arrows). Neutral position (e), Crass position (f), and modified Crass position (g).
Modified from Shah, N. P., Miller, T. T., Stock, H., & Adler, R. S. (2012). Sonography of supraspinatus tendon abnormalities in the neutral versus Crass and modified Crass positions: A prospective study. Journal of Ultrasound in Medicine, 31(8), 1203–1208. doi: 10.7863/jum.2012.31.8.1203. Wiley.
High shoulder pain prevalence is often seen in athletic pursuits, particularly those requiring forceful and repetitive motions that involve throwing or other activities where the hands and/or elbows are active above the level of the shoulder. High stresses are placed on the shoulder in activities such as baseball pitching, football throwing, tennis, volleyball, and swimming. These repetitive high‐stress activities are likely to result in microdamage and damage propagation that may exceed the repair capacity of shoulder musculoskeletal tissues (Bani Hani et al., 2021).
Subacromial impingement may also occur at the subacromial joint. It is thought to be the result of fatigue in the stabilizing structures of the shoulder (the tendons and ligaments), resulting in humeral subluxation and subsequent impingement of the supraspinatus tendon between the head of the humerus and the inferior surface of the acromion. It has been reported that the most frequent shoulder diagnoses in athletes involve RC dysfunction with signs of supraspinatus tendon impingement (Baring, Emery, & Reilly, 2007; McHardy, Pollard, & Luo, 2007; Pink & Tibone, 2000). That said, there can also be degenerative changes in the joint structure itself. In one study, the frequency of radiologically detected lesions in shoulders of 152 miners using vibration tools was 40.7% and included degenerative changes (34.5%) that were mainly in the acromioclavicular joint (17.8%) (Kakosy et al., 2006).
Upper Extremity Muscle Disorders: Fatigue, Myalgia, and Fibrosis
Characteristics/description
Muscle fatigue denotes a transient decrease in the force and power capacity of skeletal muscle activity (Enoka & Duchateau, 2008). Repetitive or sustained contraction of skeletal muscle can lead to a progressive and reversible loss in the ability to produce the desired force (Allen, Lamb, & Westerblad, 2008; Ortenblad, Lunde, Levin, Andersen, & Pedersen, 2000). Myalgia is also known as muscle pain and is a symptom of many diseases and disorders, including prolonged repetitive work (Bongers, Ijmker, Heuvel, & Blatter, 2006; Hadrevi et al., 2019; Sjøgaard, Lundberg, & Kadefors, 2000). Muscle fibrosis is characterized by fibroblast and myofibroblast cell proliferation and excessive accumulation of extracellular matrix proteins in fascial tissues, such as collagen and fibronectin (Contreras, Rebolledo, Oyarzun, Olguin, & Brandan, 2016; Fisher et al., 2015). Muscle fibrosis is also associated with increased muscle pain (Fisher et al., 2015; Pavan, Stecco, Stern, & Stecco, 2014), presumably as a secondary consequence of nerve pain receptors becoming enmeshed in the fibrosing fascial tissues (Fisher et al., 2015; Pavan et al., 2014).
Epidemiology
Prolonged standing work and intense training are associated with MSDs and muscle fatigue is considered a precursor to MSDs (Garcia, Laubli, & Martin, 2015; Hadrevi et al., 2019). However, the myriad of underlying possible reasons muscle fatigue discussed in the following section makes epidemiological studies difficult. Work‐related muscle pain (myalgia) is considered a public health problem causing otherwise healthy individuals to end up on sick leave (Holtermann, Hansen, Burr, & Sogaard, 2010). Neck pain is one of the more common MSDs, with over 30% of individuals experiencing some degree of discomfort in the neck over a lifetime (Cohen, 2015; Cote, Cassidy, & Carroll, 1998). Most episodes of acute neck pain will resolve with or without treatment, but nearly 50% of individuals will continue to experience some degree of pain or frequent occurrences. A “tissue fibrosis” hypothesis is supported by clinical studies examining biopsies from patients with chronic MSDs (Dennett & Fry, 1988; Ettema, Amadio, Zhao, Wold, & An, 2004; Hirata et al., 2005).
Anatomy/pathology
The origin of muscle fatigue (specifically, a progressive and reversible loss in the ability to produce the desired force) is complex. Muscle fatigue occurs along with physiological changes that reflect changes in the balance between muscular demand and vascular supply (Cote, 2014; Yang, Leitkam, & Cote, 2019). This latter imbalance has also been termed an “energy crisis” (Simons & Travell, 1981). Muscle fatigue can also arise with alterations in neuromuscular junctions, neurotransmitters released from peripheral nerves after tissue damage, and axonal neuropathy if compressive nerve injury develops (Zajac, Chalimoniuk, Maszczyk, Golas, & Lngfort, 2015). Chronic inflammation, which can occur after prolonged high demand tasks, has a direct deleterious effect on skeletal muscles, decreasing force and muscle quality. Persistent elevations of systemic tumor necrosis factor alpha (TNF‐α) is a primary endocrine stimulus for contractile dysfunction (Argiles, Campos, Lopez‐Pedrosa, Rueda, & Rodriguez‐Manas, 2016; Leal, Lopes, & Batista Jr., 2018; So, Kim, Kim, & Song, 2014). Dependent on the magnitude of mechanical myofiber damage, muscle strength can decline. Substantial muscle damage also induces myofiber apoptosis and a loss of muscle mass. Aging enhances muscle dysfunction due to age‐dependent increase in inflammatory responses and cell apoptosis and reduced repair mechanisms (Argiles et al., 2016). Additionally, the Cinderella Hypothesis of a hierarchical recruitment of smaller motor units disproportionately over larger units may provide insight into muscle fatigue (Enoka & Duchateau, 2008). In this hypothesis, the first recruited units are the smallest muscle units, which allow for the fine‐tuning of force applied during delicate tasks. These small motor units may also be the last to be relaxed during prolonged muscle contractions. Only as the load reaches the maximum values, larger units are recruited. Thus, the smaller fibers may be more susceptible to an energy crisis of muscle fatigue and pain signaling (Enoka & Duchateau, 2008).
Another cause of physiological muscle fatigue can be altered myocellular calcium [Ca2+] regulation, sarcoplasmic reticulum Ca2+ handling, and sarcoplasmic reticulum protein expression, all occurring as a result of chronic muscle overload, as summarized in Figure 2.7. (Allen et al., 2008; Hadrevi et al., 2019; Ortenblad et al., 2000). The process of controlling the production of force within the muscle, known as excitation–contraction–relaxation coupling, requires a tight regulation of the intracellular cytosolic free Ca2+ concentration ([Ca2+]i) in muscle enabling activation of the contractile apparatus, while protecting the cell from deleterious [Ca2+]i overload. This is permitted through an instantaneous release of large amounts of Ca2+ through the sarcoplasmic reticulum Ca2+ release channel and ryanodine receptor (RyR), thereby increasing [Ca2+]i and a subsequent, almost simultaneous reuptake of Ca2+ into the SR by the SR ATPases (SERCA) together with buffering of Ca2+ inside the sarcoplasmic reticulum by the protein calcequestrin (Casq1) (Berchtold, Brinkmeier, & Muntener, 2000; Ortenblad & Stephenson, 2003; Periasamy & Kalyanasundaram, 2007).
Figure 2.7 A model for possible early and late events in muscle response to a repetitive high repetition high force (HRHF) upper extremity task for 6 weeks. Exposure to the HRHF task induces an impaired muscle Ca2+ homeostasis, leading to an increase in [Ca2+]i as indicated by an increase in pCalmodulin kinase (pCAM). The increased [Ca2+]i