The majority of skeletal muscle injuries that occur in sports are the result of indirect strain or direct blunt force trauma. Other forms of muscular injury, such as lacerations, ischemia, and infections, are not commonly seen in athletics.
The amount of research in the area of muscle injury and repair is growing, but we do not yet fully understand the precise mechanisms behind the molecular changes that occur during muscle injury or the exact biochemical regulation of the healing response.
It appears that the postinjury release of soluble proinflammatory cytokines, growth factors, and certain free radicals from injured muscle is a central component to muscle tissue damage and repair.
Indirect muscle strain injuries usually occur at the myotendinous junction during a stereotypical eccentric contraction. Such injuries are common in athletics during the active contraction with muscle lengthening that occurs during impact absorption.
Certain muscles that perform primarily eccentric contractions during sports are more likely to sustain this type of injury. The hamstrings are particularly vulnerable during bursts of rapid acceleration, as are found in football, sprinting, and soccer.
The hamstrings function to decelerate the leg extension phase during running, combining an activated lengthening muscle contraction that predisposes these athletes to muscle strain injury. Despite the frequency of this problem in athletics, research in this area has been limited until lately. Most research models of muscle injury are patterned after this muscle activation and stretch mechanism.
Delayed muscle soreness (DMS) is a common but separate entity from pain resulting from indirect muscle strain. Onset of DMS usually occurs at least 24 hours after exercise, reaching a maximum at 48 to 72 hours. In contrast, acute muscle strain causes pain immediately.
Eccentric exercises, especially unfamiliar repetitive ones, are more likely to predispose patients to DMS. Patients often will complain of painful, stiff, and swollen muscles. A significant loss of maximal force generation often persists for up to 1 week after the original injury and for several days after the muscles are no longer painful.
Histological evidence of muscle disruption may help to explain the source of pain and the reversible loss of force generation. The exact cause of DMS pain is not known, but it appears to be related to mechanical tissue damage, not lactic acid buildup.
Direct trauma to muscles can occur at any point in the muscle. The quadriceps is the most common site of athletic muscle contusion, especially in tackle football. With sufficient force, disruption of the muscle tissue and architecture can occur, often resulting in a hematoma.
Quadriceps contusions can result in significant morbidity to athletes because of swelling and pain. Not uncommonly, calcification or ossification can occur at the site of previously contused muscle. Myositis ossificans, as it is known, is heterotopic bone formation in previously damaged muscle.
One prospective study found that approximately 20% of patients with quadriceps hematoma develop myositis ossificans . The bone formations of myositis ossificans often will regress or even disappear over time, but sometimes, it will enlarge before eventually stabilizing.
Shortly after a muscle injury, a series of events occur that produce chemoattractant signals to invading neutrophils and macrophages. In muscle strain injuries, a disruption occurs in normal fiber architecture and calcium homeostasis, leading to functional deficits as well as chemotactic substances being released from the tissue.
As quickly as 1 hour after an inciting injury, neutrophils begin migrating to the tissue, and their presence at elevated levels can last for as long as 5 days. Neutrophil presence following injury is important for removal of necrotic tissue and debris through phagocytosis; however, the neutrophils also release enzymes, such as myeloperoxidase, that promote free radical formation in the tissues during times of neutrophil invasion.
Highly reactive free radicals, such as superoxide, may directly cause damage to the surrounding tissues and cell membranes, actually promoting further damage and not repair. In fact, recent research has demonstrated that superoxide produced by activated neutrophils is capable of sarcolemma lysis in vitro, and the addition of superoxide dismutase (SOD) inhibits this muscle cell membrane lysis .
Inflammatory cytokines and trophic substances also may be produced by local endothelial tissue, macrophages, myoblasts, damaged myofibrils, and activated fibroblasts. The expression and importance of these cytokines and substances in vivo, as well as the role they play in skeletal muscle after muscle injury, remain unknown. Ongoing research will play a key role in developing new and improved strategies for the prevention and treatment of these common problems.
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