Primary injuries are the most commonly seen type of injury. The pathophysiology of each primary injury is unique in its mechanism and its resulting pathology. Our discussion will focus on the three most common primary injuries in sports medicine: contusions , lacerations, and sprains (Textbox 4.2).

Contusion injuries are the result of blunt force trauma directed into the muscle. Contusions are typically characterized by hematoma formation and only minor superficial disruption of tissue [4]. The deeper, unnoticeable damage created in contusion injuries is often of greater concern than that notable on the surface. In lacerations, the insult is a more localized, sharp dissection of tissue. The damage incurred by tissue in lacerations is often more noticeable and visually impressive than those seen in blunt injuries. However, the true extent of injury in lacerations is often more localized and, therefore, may result in less structural damage than those seen in blunt injuries. However, in the setting of large or deep penetrating lacerations, the structural damage can be quite severe. The most commonly seen primary muscle injuries are muscle strains , which represent almost half of all athletic injuries [4]. Contributing factors to strains are the magnitude of force applied, rate of force application, and the mechanical strength of the muscle unit being tested [1]. Strains are classified based on the severity of tissue disruption, degree of dysfunction, and expected return to competition. Mild strains are those with minimal or no evidence of structural damage to the muscle. Strains that result in partial tearing of the muscle, but less than full thickness, are termed moderate. Severe strains are those with full or nearly full disruption of the muscle and are associated with marked impairment of function [1]. This muscle strain classification system is an attempt to simplify the continuum of strain injuries to aid in treatment decisions and help predict timing of expected recovery. Unfortunately, there remains significant variation within each group, and this limits the clinical utility of the classification system in attempts to make more nuanced assessments .

The delayed presentation of secondary injuries can make their diagnosis more challenging than primary injuries. Examples of secondary injuries include compartment syndromes, delayed onset muscle soreness (DOMS) , and myositis ossificans. This group also includes injuries that result secondary to alterations in a person’s gait or movement patterns necessitated by compensations from the primary injury. The underlying theme in secondary injuries is that each injury is a consequence of some inciting event or pathology. Therefore, addressing secondary injuries requires identifying and optimizing treatment of the primary insult as well as addressing the secondary injury.

Compartment syndromes are characterized by pathologically increased tissue pressure within a confined space [4]. Compartment syndromes can be acute or chronic. One of the more common inciting events of acute compartment syndrome is severe blunt trauma. Blunt trauma has the potential to lead to compartment syndrome via fluid accumulation secondary to two different mechanisms. First, it may cause induction of the local inflammatory response following the traumatic event, leading to soft tissue swelling and edema. Secondly, if the trauma is severe enough, it may also cause direct compromise of vasculature within the muscle, leading to bleeding and increased severity of the resulting edema [2]. Both mechanisms result in an increase in pressure within a confined space, leading to compression of the arterioles and an ischemic insult [4]. Acute compartment syndromes are considered an acute surgical emergency .

DOMS is a secondary injury seen following repeated eccentric contractions and is distinguished by its delayed onset. DOMS is typically noticed 12–24 h postexercise and typically peaks in intensity at 48 h [3–5]. It is described as a dull ache that increases in intensity with compression, stretching of the muscle, or contraction [6]. As the name suggests, it presents as soreness of the affected muscle and is often associated with reduced range of motion and stiffness. DOMS is classically seen following repetitive eccentric exercise or activity. DOMS usually is preceded by a notable loss of force development or exhaustion in the involved muscles exhibited during exercise. However, recent investigations have produced evidence to indicate the pathology responsible for the noted force deficit seen during eccentric exercise bouts is independent of the pathologic process responsible for DOMS [3]. The pathophysiology of DOMS is not well understood, with multiple theories currently being investigated. The cause of DOMS may be a combination of several proposed mechanisms. However, the sensitization of high-threshold mechanosensitve (HTM) receptors, the primary receptors for pressure-mediated pain in skeletal muscle, likely plays a major role. HTM receptors within skeletal muscle are typically in contact with the vascular bundles and have associations with the connective tissue but do not have direct contact with myofibers [5, 6]. The sensitivity of these receptors is increased by bradykinin and serotonin, both of which are commonly released from cells during an acute inflammatory reaction. The process responsible for the propagation and release of these sensitizing agents remains controversial. It is likely that the eccentric movements, which typically precede DOMS , create enough force on the muscle to cause a disruption within the muscle itself. The location of this disruption has at least two possible locations. Connective tissue and passive elements within the muscle play a critical role in the absorption of energy created during eccentric exercise and may become damaged following unaccustomed patterns of activity. Injury to these structures may induce local inflammatory responses responsible for initiating DOMS without disruption of the other muscle tissue elements [6]. Connective tissue damage as a cause, rather than damage to myofibers, is supported by the fact that markers of myofiber injury have not correlated well with the magnitude of DOMS in multiple studies. It has also been shown that there is a significant increase in urinary hydroxyproline, a breakdown product of collagen, in subjects suffering from DOMS [7]. However, direct myofiber injury has implicated as well and is supported by studies which have shown disruption and disorganization of myofibers of muscle in subjects with DOMS [6]. While the exact mechanism of DOMS remains elusive, continued investigations into the underlying pathology will have important clinical implications for athletes and active people .

As noted above, early force deficits noted following eccentric contractions were once thought to be induced by the same pathologic process as DOMS. However, studies have repeatedly demonstrated that as repetitions increased, the magnitude of the force deficit decreased, while the magnitude of DOMS and cellular pathology continue to increase [6]. Further support for differing mechanisms between observed alterations in task performance and the pathology causing DOMS is demonstrated through the finding that by increasing the interval time between repetitions, it is possible to prevent the histological changes typically seen with repeated eccentric contractions, without the ability to prevent significant loss of force generation [8]. Both of these findings indicate that the loss of function is likely the result of a local, transient, and reversible alteration within the cell. Probable explanations include disruption in the excitation–contraction coupling mechanism or the sarcomeres themselves, which lead to ineffective contractions [6].

Myositis ossificans is a condition seen following contusion injuries in which there is subsequent calcification of the muscle [4]. The arm and anterior thigh are the most common locations, a finding mostly likely due to the fact that those locations are the most common locations for severe contusion injuries [9]. One major risk factor for myositis ossificans is early reinjury to the muscle; this finding supports a theory of altered healing response as a possible mechanism for developing myositis ossificans. Unfortunately, the pathologic process underlying myositis ossificans is still not well understood, and it remains a secondary complication of muscle injury, resulting in significant morbidity with poor treatment options [4].

Although the focus of this chapter is primarily on acute injury , chronic injuries are an important classification of muscle injuries that have a differing pathophysiologic basis and resulting pathology. Chronic inflammation is often a result of repeated trauma or incomplete recovery from injury [1]. Tissues not fully recovered from an injury have the potential to enter a cycle of chronic inflammation and recurrent damage, secondary to the inflammation and/or degeneration. The hallmarks of chronic inflammation are mononuclear cells, tissue destruction, and fibrosis [10]. The proper treatment of acute injuries and full recovery prior to return of participation is one of the best ways to prevent chronic injuries. This highlights the critical role of acute injury management as the cornerstone of diagnosis, treatment, and prevention of muscle injuries more generally .

The function of the musculoskeletal system is dependent on its structural organization. The structure, organization, and physiology of the musculoskeletal system were the focus of the preceding chapters, but here we will review a few important properties critical to the pathophysiology of muscle injuries (Textbox 4.3).

We will begin by reviewing the functional unit of muscle: the muscle fiber. The important detail of a muscle fiber is the simple fact that it is composed of multiple sarcomeres, which are the smallest contractile unit of muscle [1, 4]. Individual muscle fibers are bundled together into fascicles and arranged in various patterns. The different arrangements include parallel or pennate structures, which each have significantly different biomechanical properties. Parallel muscles can be subclassified as fusiform, fan, or strap muscles, while pennate muscles can be unipennate, bipennate, or multipennate in form. Muscles are innervated by α motor neurons that are organized into motor units controlling specific muscle fibers throughout the muscle. A motor unit consists of anywhere between 10 and more than 1000 muscle fibers, distributed throughout the muscle [4]. It is believed that the neuron itself plays an important role in determining fiber type, with each neuron innervating a homogenous population of fibers. The arrangement of sarcomeres, pattern of muscle fiber alignment, and individual motor units all impart specific biomechanical properties into muscles and are important determinants in the functional capabilities of a given muscle and also the risk for injury in that muscle.