The clinical evidence suggests that hip and pelvis dysfunction may not simply be an acute process that resolves with time alone. Typically, hip and pelvis pain and dysfunction are often a recurrent problem similar to other chronic musculoskeletal conditions that may have symptom-free periods interspersed with exacerbations. Therefore, physicians must approach hip and pelvis dysfunction with this mindset and be aware of its potential episodic, recurrent, and chronic nature. They should initially seek treatment methods that are active and physical in nature to help restore the body’s normal balance of regional and segmental joint motion, posture, and neuromuscular control, with appropriate functional strength and flexibility (SOR = B).

There are studies indicating that physical activity is a risk factor for the development of osteoarthritis of the hip and pelvis. Unfortunately, osteoarthritis of the hip is relatively common in athletes, second only to osteoarthritis of the knee. It may be the result of chronic overuse or secondary to specific traumatic events, such as transient subluxation or chondral injury [9, 10]. Kujala et al. performed a retrospective review on former elite male athletes [11]. Using a registry of Finnish male athletes who competed at an Olympic or other international level between 1920 and 1965, the study looked at relative risks of development of chronic disease. Although the participants had significant improvement in health with respect to coronary artery disease, diabetes, and hypertension, an increase in the development of osteoarthritis was noted in these athletes. The cohort was divided into endurance sports (runners and cross country skiers), mixed sports (soccer, basketball, and ice hockey), and power sports (boxing, wrestling, and weight lifting). The relative risks for osteoarthritis were 2.42, 2.37, and 2.68, respectively [11], with a 2–3 fold increase risk in females [12]. In another retrospective study, Spector et al. evaluated 81 female ex-elite middle long-distance runners and tennis players [12]. In comparison with 997 age-matched controls, the athletes demonstrated a relative risk of 2.5 for hip arthritis, and 3.5 for knee arthritis. A cross-sectional study performed by Lindberg et al. demonstrated a 5.8 % incidence of hip osteoarthritis in 286 ex-soccer players compared with a 2.8 % incidence in controls [13].

Contradicting this information are studies in long-distance runners , which fail to demonstrate an increased risk for osteoarthritis. Lane et al retrospectively studied 41 long-distance runners averaging 5 h/week of running over 9 years, concluding that there was no increased risk of osteoarthritis in runners [14]. Konradsen et al. evaluated 58 ex-long-distance runners who averaged more than 20 km\week of running over 40 years and compared them to age, weight, and occupation-matched controls. Radiographically, the athletic cohort had no significant changes suggestive of osteoarthritis when compared with controls [15].

Multiple studies have demonstrated a risk of hip osteoarthritis for professional soccer players that may be as high as 13.2 %, or 10.2 times that of the general population, even in the absence of identifiable injury to the joint [13, 16, 17]. Other studies have shown other significant increases in risk in rugby players [18], javelin throwers [19], high jumpers, track, and field sports [20]. Osteoarthritis is also common among former National Football League (NFL) players, with 62 % reporting some arthritic problem, compared to 32 % of general male population, in a 2009 NFL Player’s Care Foundation study [21]. This association of hip osteoarthritis with significant athletic activity has been demonstrated in female as well as male athletes [12, 22, 23].

Although it is not a consensus opinion of these articles, excessive microtrauma from exercise and cumulative overuse can potentially increase the risk of developing joint injury and osteoarthritis. This risk is dependent on the amount, type, and intensity of the exercise, as well as the genetics, joint structure, fitness, and body habitus of the individual [24, 25]. Other specific risk factors include high loads, sudden or irregular impact [26], and preexisting abnormalities such as dysplasia [13, 27]. More recently, labral tears of the hip have been implicated in early osteoarthritis [28].

In summary, the clinician should view athletic hip and pelvis pain and dysfunction as a common injury with a potentially episodic nature that can affect the athlete’s ability to function in both sports and personal life. Treatment must be focused on complete functional recovery and prevention, not just elimination of acute pain, as there appears to be significant risk for the development of hip arthritis if the pain and resultant kinetic chain dysfunction is left untreated (SOR = B).

Arthrokinetic responses are transmitted through the neuromuscular system as proprioceptive data processed by the central nervous system (CNS). These responses are separate from stretch reflexes, though some of the same pathways are utilized. The four nerve types responsible for transmitting afferent information from the joint are globular (static and dynamic mechanoreceptors), conical (dynamic mechanoreceptors), fusiform (mechanoreceptor), and plexus (nociceptor) [29].

The gamma loop mechanism functions in the following fashion. A dynamic load applied to the tendon stretches the spindle muscle fibers. This activates the afferent nerve fibers which synapse in the anterior horn (we are skipping the numerous interneurons for simplicity) on the alpha motor neurons in the same and adjacent spinal segments, simultaneously inhibiting the antagonist muscle groups. If the capsule or ligament becomes stretched beyond what its programming allows for as a normal range of motion (or if too rapid a stretch occurs), inhibitory signals are sent to the agonist muscle responsible for loading the joint in the plane in question and stimulatory signals to the antagonist musculature [29].

An engram is a memorized series of muscle activation patterns (MAPs), for example, tying your shoes, or changing lanes when driving a car. They free up your conscious mind from the task at hand, allowing you to focus on other tasks simultaneously. The development and “burning in” of successful engrams as well as kinetic chain movement patterns (a specific sequence of engrams resulting in a motion) result in successful athletic performance. Injuries and overload can happen when there is compensation for dysfunction (motion loss) in the earlier (temporally speaking) components of the kinetic chain and can lead to injury in the later components, as the tissues either cannot handle the load or the neuromuscular system fires inappropriately [29].

Neuromuscular imbalance in the postural musculature, either due to hypertonicity or inhibition, allows microtrauma to begin to insidiously accumulate. With repetitions of these dysfunctional MAPs, dysfunctional kinetic chains and engrams develop that “burn in” the dysfunctional, although usually asymptomatic, pathways even more. Pain and/or pathology usually will begin in the local stability system, which cannot maintain its functioning, thus perpetuating the loop [29]. Tendons and ligaments lose their tensile properties over time. Proprioceptive inputs become less reliable and actually can become harmful as MAPs and their kinetic chains are thereby altered, leading to abnormal loading of bone and the supporting soft tissues.

Much of our understanding of the biomechanics of the hip joint has been obtained through simple static diagrams, gait analysis, and through the insertion of force-measuring implants . The muscles about the hip joint are generally at a mechanical disadvantage because of a relatively short lever arm and a production of forces across the joint that are several times body weight. It has been calculated that level walking can produce forces of up to six times body weight and that jogging with a stumble increases these forces to up to eight times body weight [30]. Although forces, when measured in vivo, tend to be less than the calculated values, one can anticipate potentially greater loads during vigorous sports athletic competition [31]. The structures about the hip are uniquely adapted to transfer such forces. The body’s center of gravity is located within the pelvis, anterior to the second sacral vertebra; thus, the loads that are generated or transferred through this area are important in virtually every athletic endeavor [32].

The normal hip joint is capable of a flexion and extension arc of approximately 140°, but one study has shown that slow-paced jogging used only about 40° of this arc [33]. This increases somewhat as pace increases. Analysis of electromyographic. (EMG) activity shows that the rectus femoris and iliac muscles are very active with swing-phase hip flexion, while the hamstring muscles act eccentrically to control hip flexion and decelerate knee extension [34]. It is of note that, when running, the body is propelled forward primarily through hip flexion and knee extension rather than by push-off with ankle plantar flexion.

Sahrmann has described a hip lateral rotation (HLR) movement impairment that she has observed in people with LBP [35]. The impairment is described as early coupling [36, 37] of the primary hip rotation motion with lumbopelvic rotation during a clinical test of active HLR in prone position [38]. The HLR test was performed with the patient in the prone position, the knee flexed to 90°, and the hip in neutral rotation and neutral abduction/adduction. At a self-selected movement speed, patients laterally rotate the hip as far as possible toward the opposite leg, and then return it to the starting position. This is done both actively and passively and the amount and quality of the motion is noted by the clinician [35]. The relationship between LBP and repeated early coupling of hip and lumbopelvic rotation may be of particular importance in people who put rotational demands on both the hip and lumbopelvic region [35]. Passive tissue stiffness about the hips has the potential to contribute to early motion of the lumbopelvic region during HLR [37].

Patients may, therefore, demonstrate lumbopelvic-coupled movement early during HLR because they have a greater amount of passive stiffness in the hip musculature. The difference in the pattern of movement during the HLR test may be the result of an interaction of biomechanical factors, such as passive tissue stiffness, and motor control factors, such as timing and magnitude of muscle activity. Identifying how movement patterns differ during this clinical test is important because it provides information that can assist the clinician in treatment of a person with hip and pelvis pain and dysfunction.

Atraumatic instability can occur because of overuse or repetitive motion. This is a common complaint in athletes who participate in sports involving repetitive hip rotation with axial loading (i.e., figure skating, golf, football, baseball, martial arts, ballet, gymnastics, etc.). The history provides the greatest clues to the diagnosis because patients can usually describe the motion that causes the pain, such as swinging a golf club during a drive or throwing a football. These repetitive stresses may directly injure the iliofemoral ligament or labrum and alter the balance of forces in the hip. These abnormal forces cause increased tension in the joint capsule, which can lead to capsular redundancy, painful labral injury, and subsequent microinstability. On physical examination, patients will usually experience anterior hip pain while in the prone position with passive hip extension and external rotation [39, 40].

Once the static stabilizers of the hip, including the iliofemoral ligament and labrum, are injured, the hip must rely more on the dynamic stabilizers to maintain stability during activity. It is hypothesized that when capsular laxity is present, the psoas major, a dynamic stabilizer of the hip, contracts to provide hip stability. Over time, this condition can lead to stiffness, coxa saltans, or flexion contractures of the hip [41, 42]. In addition, because of the origin of this muscle from the lumbar spine, a chronically contracted or tightened psoas major may be a major contributor to LBP . Thus, hip instability or capsular laxity can trigger a whole spectrum of disorders that the physician must take into consideration when considering various treatment options [37].

The relationship between hip rotation motion, hip stability, and LBP is important because external forces must be sequentially transmitted from distal body segments to more proximal ones during movement. Movement at the hip could, therefore, influence movement and loading at the lumbar spine. When performed repeatedly, such hip movement could result in excessive loading on tissues in the low back region, and eventually LBP [35].

In 2001, Vleeming et al. [43] described their integrated model of joint dysfunction . This functional description comes from extensive study of the sacroiliac joint (SIJ) over the past 10–15 years, and is the most studied and supported model for sacroiliac joint dysfunction (SIJD) . It integrates structure (form and anatomy), function (forces and motor control), and the mind (emotions and awareness) on human performance. Integral to the biomechanics of SIJ stability is the concept of a self-locking mechanism. The SIJ is the only joint in the body that has a flat joint surface that lies almost parallel to the plane of maximal load. Its ability to self-lock occurs through two types of closure—form and force.

Form closure describes how specifically shaped, closely fit contacts provide inherent stability independent of external load. Force closure describes how external compression forces add additional stability (Fig. 3.2). It had long been thought that only the ligaments in this region provided that additional support. However, it is the fascia and muscles within the region that provide significant self-bracing or self-locking to the SIJ and its ligaments through their cross-like anatomic configuration. Ventrally, this is formed by the external abdominal obliques, linea alba, internal abdominal obliques, and transverse abdominals, whereas dorsally the latissimus dorsi, thoracolumbar fascia, gluteus maximus, and iliotibial tract contribute significantly. In addition, there appears to be an arthrokinetic reflex mechanism by which the nervous system actively controls this added support system. These supports are critical in asymmetric loading, when the SIJ is most prone to subluxation. The important concept to gain from this understanding of integrated function with regard to treatment and prevention of LBP is that SIJD is a neuromyofascialmusculoligamentous injury [1].

The relationship of the abdominal musculature and the erector muscles of the spine, along with their role in stabilization of the lumbosacral spine, is being studied extensively because of the high incidence of LBP in our society. Decreased spinal mobility and trunk muscle strength have been identified in patients with recurrent LBP [44]. These muscles must also be considered for their role in conditions that affect pelvic tilt and the hip joint. The transversus abdominis has been shown to be the key muscle to functional stability of the lumbosacral pelvic region to generate stability and retraining of the core, because of its observed patterns of firing before and independent of the other abdominal muscles. Most recently, a study by Richardson et al. [45] appears to show that these clinical benefits focusing on the transversus abdominis occur as a result of significantly reduced laxity in the SIJ. The balance of the muscles of the upper thigh, particularly the adductor muscles, with those of the lower abdomen requires further study. Conditioning programs have traditionally focused on strengthening of the extremities. Only recently have there been rehabilitation programs designed to address the power and endurance of the trunk and postural muscles [46, 47].

Vleeming et al. [48] defined the posterior layer of the thoracolumbar fascia as a mechanism of load transfer from the ipsilateral latissimus dorsi and the contralateral gluteus maximus. This load transfer is critical during rotation of the trunk, helping to stabilize the lower lumbar spine and pelvis. This was demonstrated through cadaveric and EMG studies [49]. The stretched tissue of the posterior thoracolumbar fascia assists the muscles by generating an extensor influence and by storing elastic energy during lifting to improve muscular efficiency [1].

In recent years, intramuscular EMG studies of the hip flexor muscles during human locomotion have revealed a separate role of the psoas and iliacus muscles for stability and movement of the lumbar spine, pelvis, and hip [49–51]. In 1995, Vleeming et al. presented evidence that the iliacus muscle was selectively recruited in the standing position with extension of the contralateral leg, and in standing, maximal ipsilateral abduction, significantly higher levels of activation in the iliacus muscle, when compared with the psoas muscle, were found [48]. This suggested preferential action of involved single-joint muscles when possible to achieve local pelvic control . In another study, Anderson et al studied walking and running and found that the iliacus muscle was the main “switch muscle” during low-speed walking [49]. Therefore, it is the key to reversing lower extremity motion from extension to flexion. In a later study, they reported that the iliacus and sartorius muscles performed a static function needed to prevent a backward tilting of the pelvis during trunk flexion sit-ups [51]. Also, with static supine leg lifts, there was progressively more activation of these muscles with increasing elevation of the extremity; they recognized that a change in pelvic tilt influenced activation of the iliacus and sartorius muscles. A backward pelvic tilt combined with a hypolordotic back decreased activation of these muscles, whereas forward pelvic tilt combined with a hyperlordotic back increased activation of these muscles. This suggests an important and separate role of the iliacus from the psoas in function and dysfunction of the low back and pelvis region [50].

Recent studies show there is both a functional and anatomic connection between the biceps femoris muscle and the sacrotuberous ligament [52–54]. This relationship allows the hamstring t o play an integral role in the intrinsic stability of the pelvis and SIJ. It appears that the biceps femoris, often found to be short on the pathologic side in LBP , may actually be a compensatory mechanism via the previously described arthrokinetic reflexes to help stabilize the SIJ. In healthy individuals, a normal lumbopelvic rhythm exists, during which the first 65° of forward bending is via the lumbar spine, followed by the next 30° via the hip joints. Increased hamstring tension prevents the pelvis from tilting forward, which diminishes the forward bent position of the spine, which results in reducing the spinal load [54]. Normalization of the lumbopelvic rhythm is an essential component to treatment of LBP, hip, pelvis, and SIJD [1].

In the normal gait cycle (see Chap. 4: Gait Assessment), there are combined activities that occur conversely in the right and left innominates and function in connection with the sacrum and spine (Fig. 3.3) [55]. As one steps forward with the right foot, at heel strike the right innominate rotates posterior and the left innominate rotates anterior. During this motion, the anterior surface of the sacrum is rotated to the left and the superior surface is level, while the spine is straight but rotated to the left. Toward mid-stance, the right leg is straight and the innominate is rotated anterior. The sacrum is rotated right and side-bent left, while the lumbar spine is side-bent right and rotated left. At left heel strike, the opposite sequence will occur and the cycle is repeated. Throughout this cycle, there is a rotatory motion at the pubic symphysis, which is essential to allow normal motion through the SIJ. Several authors [56, 57] have suggested that pubic symphysis dysfunction in walking is one of the essential or leading causes of the development of hip and pelvic dysfunction. In static stance, the lumbar spine regionally extends (i.e., lumbar lordosis), the sacrum regionally flexes, with the base moving forward and the apex moving posterior. During forward bending, both innominates go into a motion of external rotation and out-flaring. This combination of motion during forward bending is called nutation of the pelvis . The opposite occurs in backward bending, which is called counter-nutation . As the sacrum goes into extension with the base moving posterior and the apex anterior, the innominate components internally rotate and in-flare. This motion is clearly demonstrated and illustrated by Kapandji [58].

The model of suboptimal posture, though incomplete, has shown to be effective when used as a model to guide treatment [59–61]. Posture can be defined as the size, shape, and attitude of the musculoskeletal system with respect to gravitational force [62]. Subtle departure from ideal posture has been implicated as an important biomechanical factor in athletes with regard to injury because it results in increased mechanical stress throughout the body. Posture must always be evaluated as part of the biomechanical evaluation. The size, shape, and attitude of three cardinal bases of support should always be included—standing surface, the feet, and the base of the sacrum [1].

Muscles respond to dysfunctional joints in a predictable, characteristic pattern. This pattern is not random and occurs irrespective of the clinical diagnosis or specific regional injury. Tonic or postural muscles are facilitated and hypertonic, which maintain a low level of tone nearly all the time. These muscles tend to utilize more fibers of an oxidative nature to avoid fatigue. Phasic or dynamic muscles are inhibited, hypotonic, or “weak” (pseudoparesis). They exhibit quicker, shorter bursts of activity with phases of rest in between and more often utilize the glycolytic pathway fibers [33]. The specific response pattern of the muscles in the lower half of the body is seen in Fig. 3.4.

Tonic muscles will increase their resting tone and become less pliable. Phasic musculature will become less responsive and weak. Both responses will carry negative impact for the kinetic chain resulting in compensatory phenomenon. This muscle dysfunction, referred to as neuromuscular imbalance, is characterized by a change in the sequence of MAPs . This has been described both as an upper crossed syndrome and a lower (pelvic) crossed syndrome that when combined produce a layered syndrome that can be appreciated throughout the body (Fig. 3.2). Superficial and deep EMG analysis reveals that there are delays in the activation of phasic muscles, a decrease in amplitude, and recruitment of phasic muscles, and that normal input can have an inhibitory effect [63].

Triggers of muscle imbalance patterns include muscle disuse, repetitive movements, development of inflexibility, and pain. Of these, pain seems to be the single dominant factor in the maintenance of these patterns. Muscle imbalance should be suspected any time there are abnormal firing sequences on range-of-motion testing, poor balance, recurrent somatic dysfunction, “weak” or easily fatigable phasic muscles on clinical exam, history of recurrent injury or other overuse injury in the same region, chronic pain, and postural imbalance. It is critical to understand these muscle imbalances because they may be a dominant factor in the cause of musculoskeletal pain and/or a major factor in the continuance of the pain. Failure to rehabilitate these patterns is sure to be a significant factor in recurrent injury [63].

Initially the pseudoparesis, as described above, may be seen as a CNS inhibition, not a true weakness. Over a prolonged time period of inhibition, the muscles actually may become weak. Attempts at strengthening the “weak” muscles only increase inhibition. Physiologically, a decrease in recruitment is seen with added resistance. These muscles actually may not appear grossly weak on initial testing but they are seen to fatigue quickly and demonstrate poor endurance. This can lead to poor motor control or neuromuscular instability, in which there is marked irregularity in sensory-motor balance . It is important to remember that treatments and rehabilitation must be directed at the cause of inhibition, the neural reflex, first as most likely this will be a major factor in recurrent injury.

In a review from by Rankin et al, between 2006–2011 in nearly 900 soccer, rugby, football, and running athletes, they found the largest etiology of hip and pelvic pain was 56 % joint related. They further delineated between specific etiologies (joint, adductors, iliopsoas, and stress related injuries) and compared between males and females. In females, 77 % were related to the joint specifically, followed by 17 % iliopsoas, 4 % pubic bone stress related injuries, and 3 % adductor injuries. While in men, 45 % were joint related, followed by 22 % adductor, 19 % pubic bone stress related, and 6 % iliopsoas [64].

Strains of the adductor group (adductor longus, magnus, and brevis; gracilis; pectineus; and obturators) are the most common causes of acute groin pain in athletes. Their primary function is stabilization of the lower extremity and pelvis in the closed kinetic chain, as well as adduction of the thigh in the open kinetic chain and assisting in femoral flexion and rotation [65]. Strains are more common with eccentric loading. The adductor longus is most frequently affected, at the musculotendinous junction, likely because of its lack of mechanical advantage [66].

Among soccer players, incidence rates ranging between 10 % and 18 % have been reported [55, 67, 68]. Risk factors associated with increased incidence of strains include decreased hip range of motion, decreased adductor strength, and prior injury with 32–44 % of injuries classified as recurrent [69–72]. In addition, biomechanical abnormalities of the lower limb, such as leg-length discrepancy, imbalance of the surrounding hip musculature, and muscular fatigue, have also been postulated to increase the risk of adductor strain [71]. Although there have been no controlled clinical studies proving these latter elements to be causative, prevention programs focused on ameliorating some of these abnormalities have been shown to be effective in professional hockey players [73].

In 2002, National Hockey League (NHL) statistics demonstrated that adductor strains occurred 20 times more frequently during training camp as opposed to the regular season, implying that deconditioning might contribute to these injuries, and therefore, functional sport-specific strengthening programs may be preventative. Such strengthening of the musculature of the hip, pelvis, and lower extremities has long been thought to be an important part of adductor injury prevention programs [74]; recently, these programs have been documented to be effective in preventing groin injuries in soccer and hockey players [72, 75]. In one study, Tyler et al. [72] presented their strengthening and injury prevention programs focused on decreasing adductor weakness (with a goal of keeping at least 80 % of abductor strength). They found that adductor strengthening significantly reduced injury in NHL players.

Strains and tendonitis of the iliopsoas muscle usually occur at the musculotendinous junction during resisted hip flexion or hyperextension. Iliopsoas bursitis can occur alone or in conjunction with strain. The two conditions commonly occur concomitantly and are essentially identical in their clinical presentations [76]. The iliopsoas bursa is the largest bursa in the body. It communicates with the hip joint in 15 % of people and can be a source of significant groin pain. Bursitis results from overuse and friction as the tendon rides over the iliopectineal eminence of the pubis (Fig. 3.5). This condition occurs in activities requiring extensive use of the hip flexors including soccer, ballet, uphill running, hurdling, and jumping. Iliopsoas bursitis is characterized by deep groin pain that sometimes radiates to the anterior hip or thigh and is often accompanied by a snapping sensation. If this is severe enough, the athlete may exhibit a limp [77]. Because of poor localization and reproducibility of the pain, the average time from the onset of symptoms to diagnosis has been reported from 32 to 41 months [76].