Muscle and Tendon Injury and Repair
Luis P. Carrilero
Bradley J. Nelson
Dean C. Taylor
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SKELETAL MUSCLE INJURY AND REPAIR
Muscle injury is the most common musculoskeletal complaint in the athlete. Common muscle injuries include muscle strains, delayed muscle soreness, contusions, and cramps. Muscle injury results in 15%-50% of all injuries sustained in sports. More than 90% of these frequent injuries are contusions and strains, whereas laceration is considered the least frequent (20,27).
Anatomy and Physiology
Skeletal muscle is composed primarily of contractile proteins (myosin and actin), regulatory proteins (tropomyosin and troponin), and a connective tissue matrix (13).
The muscle fiber is the basic structural element of skeletal muscle. Muscle is a syncytium of multinucleated fibers (17). The functional unit of muscle is the sarcomere. Within each sarcomere are light and dark bands. The dark bands are made up of both the thick myosin and thin actin filaments, whereas the light bands are made up of just the thin actin filaments that connect to the Z lines.
A muscle fiber originates via a tendon from bone, traverses one or more joints, and joins with a tendon that inserts to bone. Fiber arrangement can be parallel or oblique (unipennate, bipennate, multipennate) in orientation. Fibers can be classified as Type I (slow-twitch oxidative) and Type II (fast-twitch). Type II fibers are further classified into Type II (fast-twitch oxidative glycolytic) and Type IIb (fast-twitch glycolytic).
Satellite cells are separate cells along the periphery of the muscle fiber that are important in cellular regeneration in response to injury. Satellite cells proliferate and transform into myotubes in response to growth factors and cytokines that mediate the repair process (62).
The musculotendinous junction is a specialized region of highly folded membranes that increase the surface area for force transmission (13). Most muscle strain injuries occur in this region.
The sarcoplasmic reticulum is a specialized cellular organelle that is responsible for calcium movement across the cell membrane and electrical transmission within the cell.
A motor unit is a motor neuron and all the muscle fibers it innervates. The motor neuron innervates each of its muscle fibers at a motor end plate. The number of myofibers in a motor unit and the number of motor units in a skeletal muscle are determined by the function of the muscle (20). The fewer the fibers in a motor unit, the finer is the control (e.g., ocular muscles), whereas many fibers in a motor unit lead to gross movements (e.g., quadriceps).
A muscle contraction begins when an electrical impulse travels down a motor neuron’s axon to its motor end plates. This electrical impulse triggers the release of acetylcholine that migrates to receptors on the myofiber and causes a depolarization of the sarcolemma. The depolarization travels deep into the muscle by the transverse tubule, triggering the release of calcium from the sarcoplasmic reticulum. Calcium binds to troponin, which results in a conformational change in the tropomyosin, opening actin’s active site and allowing the crossbridges of the myosin head to interact. The crossbridges then undergo their own conformational change that pulls the thin actin filament to slide past the myosin toward the center of the sarcomere. The process of sarcolemmal depolarization and the resulting sliding of the filaments is referred to as excitation-contraction coupling. The physical process of muscle contraction is the sliding of the actin filament past the myosin filament toward the center of the sarcomere pulling the ends of the sarcomere (the Z lines) toward each other. The whole muscle shortens when the process is multiplied over thousands of sarcomeres, thousands of conformational changes at the myosin crossbridge heads, and all of the activated fibers. This process is powered by the hydrolysis of adenosine triphosphate (ATP) to both bind and break the connection of the crossbridge with the actin filament (17,20).
Muscle contraction can be isometric, concentric, or eccentric. Isometric contraction is when the force by the muscle is equal to the load, and although there is no visible joint movement, the muscle does shorten. By recruiting more muscle fibers to overcome the external load, a concentric (or shortening) contraction can occur, and there is visible joint movement. Eccentric contraction is when the external load is greater than the force generated by the muscle and the muscle lengthens (20). For example, raising the weight in an
arm curl is a concentric contraction of the elbow flexors, and lowering the weight is an eccentric contraction of the same flexors. Isometric strength measurements are strongly predictive of functional capacity and are sensitive in detecting changes in muscle strength (36).
The pathophysiology of the healing muscle is similar regardless of the type of injury. Healing occurs in three distinct phases: (a) degeneration and inflammation; (b) muscle regeneration; (c) development of fibrosis (20). The reparative process involves both inflammatory cells (neutrophils, macrophages) and myogenic (satellite) cells.
Acute hemorrhage and inflammatory cell infiltration of the damaged muscle tissue occurs shortly after injury (40).
Initially, neutrophils infiltrate the injury site via cellular chemotaxis. Mediators such as basic fibroblast growth factor (BFGF), platelet-derived growth factor (PDGF), and interleukin-1 (IL-1) regulate myoblast proliferation and differentiation to foster regeneration and repair of the muscle, as well as stimulation of macrophages and fibroblasts within the muscle tissue (17,20).
Macrophages are the most prevalent inflammatory cells present in injured muscle. Distinct subclasses of macrophages have been identified and play specific roles in the healing process. One subclass of macrophages is involved in the phagocytosis of damaged tissue and further stimulation of the inflammatory response. A second subclass of macrophages helps modulate the reparative process (61).
Satellite cells are myogenic mononuclear cells responsible for muscle fiber repair and regeneration processes. They are located beneath the basal lamina of skeletal muscle fibers. Mechanical or chemical insults stimulate quiescent satellite cells through hepatocyte growth factor (HGF)/nitric oxide radical-dependent pathways (3,53). The activated satellite cells enter the cycle cell and differentiate into myoblasts, which fuse together and develop into multinucleated muscle fibers. Typically, these repaired myofibers attach to the extracellular matrix of the newly formed scar (32).
Fibroblast proliferation and collagen matrix synthesis occur along with the inflammatory response and muscle regeneration. This connective tissue scar formation may inhibit the complete repair of injured muscle (32). Muscle degeneration and inflammation occur during the first days after injury. Regeneration then starts after 1 week, peaks at 2 weeks, and is typically complete by 3-4 weeks. Scar tissue starts to form 2-3 weeks after injury and increases (18).
There has been considerable muscle-derived stem cell (MDSC) research recently, and the literature provides evidence that stem cells participate in myofiber regeneration. In addition, these pluripotent stem cells can differentiate into endothelial and neural lineages, which may be beneficial in vascular and neural supply to the regenerating muscle. MDSCs have also been used to produce proregenerative and antifibrotic agents (18). However, the medical evidence in humans is limited, and further studies are needed.
Muscle Strain Injury
Muscle strain is the most common injury sustained in sports. Muscle can be functionally limited from delayed muscle soreness (discussed later), partial muscle strain, or complete muscle disruption.
A common feature in muscle tissue injury is muscle stretch in combination with a strong contraction in two-joint muscles (e.g., rectus femoris, biceps femoris, gastrocnemius) or muscles with a complex architecture (e.g., adductor longus). The injury occurs when selected muscles restrict range of motion of the joint they cross and a significant amount of tension is placed on that muscle (40).
Clinically, muscle injury (strain/contusion) is classified depending on the level of damage generated: mild when the loss of strength and movement is minimal or nonexistent, moderate with inability to contract, and severe for absolute loss of function (22).
Mechanism of Injury
Although a concentric muscle contraction alone is insufficient to create muscle strain injury, the force per fiber is higher in the relatively few muscle fibers needed during eccentric muscular contraction. The combination of passive stretch of the muscle past its resting length, eccentric loads, and the subsequent concentric contraction is required to injure the muscle (16). This overextension and tension development can then disrupt the myofibers near the myotendinous junction (26).
Cellular disruption results in the hydrolysis of structural proteins and inflammation that further damages the muscle tissue (39).
Animal studies reveal that muscle tissue sustaining a nondisruptive strain injury demonstrates decreased load to failure when subjected to stress (41,60). In addition, these partially injured muscles generate significantly less contractile force, which contributes to the clinical observation that significant muscle strain injuries are frequently preceded by a minor injury. These studies also underscore the importance of rest and complete recovery prior to the resumption of athletic activities.
Diagnosis and Imaging
Although reviewing the athlete’s history is essential, tenderness to palpation at the myotendinous junction is hallmark. When a complete rupture is present, a defect may be palpated, and weakness should be expected.
Ultrasound, due to its lower costs and portability, is sometimes the first diagnostic modality. Evaluation of superficial structures such as the patellar tendon is easier with ultrasound; however, in athletes with a voluminous musculature, the evaluation of deep structures may be difficult due to dissipation of the sound waves and the lack of reflection over long distances (4).
Magnetic resonance imaging is typically unnecessary for diagnosis of muscle strain, but it may help determine the severity of the strain, continuity of the myotendinous junction, and possible convalescent time, which is crucial for elite athletes. T1-weighted images show excellent anatomic detail such as the myotendinous junction disruption, whereas T2-weighted images are fluid-sensitive and reveal pathologic processes involved in edema, making muscle strains easy to visualize (4,40).
Similar to general reparative response of muscle described earlier.
The presence of inelastic fibrotic tissue (scar) may make the muscle more susceptible to additional injury.
Treatment and Prevention
Reduced activity is key in the treatment of muscle strain injuries. This helps control inflammation and prevents further tissue damage.
The RICE principle (rest, ice, compression, and elevation) should be implemented immediately after skeletal muscle injury. Immobilization can diminish pain, reduce inflammation, and allow torn muscle ends to reapproximate. Prolonged muscle immobilization (> 7-14 days) results in lower loads to failure and should be avoided. Early motion also limits adhesions and provides quicker proprioceptive recovery (40).
Therapeutic ultrasound is thought to relieve pain and promote muscle regeneration during the initial phase of muscle injuries. Its recommendation and use is promoted even though the results from animal studies have not been encouraging. In addition, its effectiveness in the complete healing process is questionable (47,64).
Clinical trials have failed to demonstrate the benefits of hyperbaric oxygen therapy in the treatment of mild muscle injuries in athletes (12).
Nonsteroidal anti-inflammatory drugs
Animal studies demonstrate that nonsteroidal anti-inflammatory drugs (NSAIDs) reduce the inflammatory response associated with muscle strain injury, providing more complete functional recovery by 1 week. A certain level of inflammation is necessary, however, to remove necrotic tissue and permit healing; thus, NSAIDs may delay complete healing of the damaged muscle tissue (39,41). The indication for the use of these drugs in muscle strain injury is unclear, and many physicians recommend only a short course of NSAIDs immediately after the acute strain (40).
Muscle strengthening is an important factor in the recovery of injured muscle and the prevention of reinjury. Eccentric muscle strengthening exercises have been shown to decrease the rate of hamstring injuries in studies that compare conventional and eccentric strengthening exercises (6,7,14,15).
The gradual return to training activity should be considered when the athlete is able to stretch the injured muscle as far as the contralateral muscle and denies pain with basic movements (44). One prospective randomized study on hamstring strains highlighted that exercises of progressive agility and trunk stabilization resulted in fewer reinjuries and accelerated the return to practice of the athlete when compared to a stretch and strength protocol (54).
Muscle stretching and warm-up
Muscle is viscoelastic material, and passive stretching can reduce stress for a given muscle length (59). In addition, preconditioned muscle and warm muscle fail at higher loads than control muscle (49). A recent review stated that a warm-up and stretching protocol implemented within the 15 minutes prior to starting physical activity results in better performance scores and fewer muscle injuries (67).
A systematic review of clinical and basic science literature, however, questioned this conclusion, stating that an intense period of stretching prior to exercise did not improve the athlete’s performance, failed to prevent muscle injuries, and may make the muscle more susceptible to injury (55
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