Facial Fractures

Background

Facial fractures occur for a variety of reasons related to sports participation: contact between players (eg, a head, fist, elbow); contact with equipment (eg, balls, pucks, handlebars); or contact with the environment, obstacles, or a playing surface (eg, wrestling mat, gymnastic equipment, goalposts, trees). Direct body contact accounts for the majority of sports-related injuries, and the most commonly associated soft tissue injuries were found in the head and neck region.[1]

Although most sports-related facial injuries are minor, the potential for serious damage exists. A physician examining these injuries must rapidly assess the patient in a consistent and methodical manner, allowing for prompt diagnosis and appropriate treatment, while considering the physical demands of the sport, as well as the athlete's return to play.

Facial fractures may be associated with head and cervical spine injuries.[2, 3] A review by Boden et al of catastrophic injuries associated with high school and college baseball demonstrated 1.95 direct catastrophic injuries annually, including severe head injuries, cervical injuries, and associated facial fractures.[3]

Fractures of the facial bones require a significant amount of force. The physician must take into account the mechanism of the injury as well as the physical examination findings when assessing the patient.

Forces that are required to produce a fracture of the facial bones are as follows:

Nasal fracture – 30 gZygoma fractures – 50 gMandibular (angle) fractures – 70 gFrontal region fractures – 80 gMaxillary (midline) fractures – 100 gMandibular (midline) fractures – 100 gSupraorbital rim fractures – 200 g

For patient education resources, see the Back, Ribs, Neck, and Head Center; Breaks, Fractures, and Dislocations Center; Sports Injury Center; Eye and Vision Center; and Teeth and Mouth Center.

Also, see Facial Fracture, Broken Nose, Broken Jaw, Concussion, Black Eye, and Broken or Knocked-out Teeth.

NextEpidemiologyFrequencyUnited States

In 1977, Schulz noted that athletic injuries account for 11% of all facial fractures and that facial injuries occur in 2% of all athletes.[4] More recently, Reehal noted that facial fractures accounted for 4-18% of all sports injuries.[5] A review by Romeo of facial fractures sustained by athletes during sports participation noted that sporting activities account for 3-29% of facial injuries and 10-42% of all facial fractures.[6] Tanaka and colleagues showed that 10.4% of all maxillofacial fractures are related to sports.[7]

In another report, Laskin stated that 250,000 individuals, many of whom were children, experience facial trauma while engaged in athletic activities.[8] The review by Hwang et al demonstrated that athletes aged 11-20 years were the population that accounted for most (40.3%) sports-related facial bone fractures.[1] Additionally, it is estimated more than 100,000 sport-related injuries could be prevented by wearing appropriate head and face protection.[8]

Retrospective analysis demonstrated a significant male predominance (13.75:1) among athletes who sustained sports-related facial bone fractures.[1] The sports most commonly associated with facial fractures were soccer (38.1%), baseball (16.1%), basketball (12.7%), martial arts (6.4%), and skiing/snowboarding (4.7%).[1]

Nearly 75% of facial fractures occur in the mandible, zygoma, and nose.[9] Sports participation is the most common cause of mandibular fractures (31.5%), followed closely by motor vehicle accidents (27.2%). A study of facial fractures sustained during recreational baseball and softball demonstrated that the zygoma or zygomatic arch was the most common fracture subtype, followed by temporoparietal skull fractures and orbital blow-out fractures.[10] A number of studies in the medical literature, however, indicate that the nasal bones are the most commonly fractured bones in the face, but because many of these patients do not seek medical treatment or the injuries are managed in the outpatient setting, the statistics may not reflect this trend.[2] It is likely that the nasal bones are more commonly fractured because of the lesser degree of force that is required to fracture the bone.[11]

Fractures of the orbit occur more commonly in young adult and adolescent males: the mean age for adult males is 32 years; the mean age for children, 12.5 years, and the majority of orbital fractures occur in boys. In addition to sports-related injuries, injuries sustained in motor vehicle collisions, assaults, and occupational injuries account for the majority of orbital fractures.[12]

PreviousNextFunctional Anatomy

Frontal sinus: Both the anterior and posterior wall may be damaged. Because the posterior wall is adjacent to the dura mater, damage in this region could result in central nervous system (CNS) complications such as a cerebrospinal fluid (CSF) leak or meningitis.

Orbital: The bony orbit (see image below) is composed of 7 bones of varying thickness. The frontal bone forms the supraorbital rim and orbital roof. The medial surface consists of the ethmoid, whereas the greater wing of the sphenoid and the zygoma create the lateral margin. Inferiorly, the floor and infraorbital rim are formed by the zygoma and maxilla. This portion is very thin; therefore, it is the most common site of fracture within the orbit. Fracture of the orbital floor, also known as a blow-out fracture, can result in entrapment of the inferior rectus muscle, limiting upward gaze.

The bony walls of the orbit.

The most common fracture to the orbital rim involves the orbital zygomatic region; this fracture, which typically results from a high-impact blow to the lateral orbit, often results in a fracture to the orbital floor as well.[12]

Nasal: The nose is the most prominent feature of the facial structures and is the most commonly fractured of all facial bones.[5] The upper third of the nose is supported by the paired nasal bones and the frontal process of the maxilla, whereas the lower two thirds of the nose are maintained by cartilaginous structures.[11] A more serious injury, a nasoorbitoethmoid fracture, occurs with trauma to the bridge of the nose. This injury involves extension into the frontal and maxillary bones and can result in disruption of the cribriform plate with concomitant CSF rhinorrhea.

Zygomatic/zygomaticomaxillary complex: The zygoma, like the nasal bones, is a prominent facial bone and, therefore, is prone to injury. Commonly, a breakage in this area involves a central depression with fractures at both ends. The central fragment may impinge upon the temporalis muscles, resulting in trismus. Because of its thickness, isolated fractures of the zygoma are rare, often involving extension into the thinner bones of the orbit or maxilla, otherwise known as zygomaticomaxillary (ie, tetrapod or tripod fractures).

Maxillary (Le Fort): Rene Le Fort first described fractures of the maxillary region in the 1900s (see image below). Classification of maxillary fractures is based on the most superior level of the fracture site.[5]

Le Fort fractures.

Le Fort I injuries involve a transverse fracture of the maxilla above the level of the root apices and through or below the level of the nose.

Le Fort II injuries traverse the nose, infraorbital rim, and orbital floor and then proceed laterally through the lateral buttress and posteriorly through the pterygomaxillary buttress.

Le Fort III injuries, also known as craniofacial dysjunction, result from motor vehicle or motorcycle accidents and are the result of the mid face being separated from the cranial base.

Mandibular: Fractures of the mandible (see image below) can involve the symphysis, body, angle, ramus, condyle, and subcondyle regions. Fractures of the mandibular body, condyle, and angle occur with nearly equal frequency, followed by fractures of the ramus and coronoid process.[5] Generally, motor vehicle accidents result in fractures of the condylar and symphysis regions because the force is directed against the chin, whereas injuries from boxing are more likely to be located in the mandibular angle, as the result of a right-handed punch. Over 50% of mandible fractures are multiple; the presence of one mandibular fracture mandates evaluation for additional fractures, perhaps contralateral to the affected side.[5]

Mandibular fractures. PreviousNextSport-Specific Biomechanics

In general, facial fractures in athletic activities result from direct trauma over a small surface area. Sports that present a higher risk are those that involve small objects that are propelled at high velocity, such as baseball, softball, hockey, lacrosse, jai alai, and racquetball. Athletes who participate in sports with high levels of physical contact and collision are at risk as well; these sports include football, basketball, rugby, hockey, martial arts, and boxing.

Many of these sports have safety measures to limit the incidence of facial injuries, and attention should be paid to the rules of use. Racquetball players should always play with goggles to limit orbital blow-out injuries. In hockey, face guards with helmets are required in lower levels of play but not at the professional level. High school football players should all have mouthpieces fitted for them, and mouthpieces should be worn in place before every play.

An athlete's vision should be checked as part of a preparticipation physical examination yearly. Visual risk factors include a corrected visual acuity of 20/40 or less or spectacle correction greater than 6 diopters (D). These athletes need an ophthalmologist's evaluation before competing in sports.

A one-eyed athlete is defined as one with a visual acuity in one eye of 20/200 or less. These athletes may be able to participate with proper protection, and an ophthalmologist's evaluation is essential.

PreviousProceed to Clinical Presentation , Facial Fractures

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Athletic Foot Injuries

Background

Athletic foot injuries can be difficult to properly diagnose and treat. Bearing the weight of the entire body, the foot is under tremendous stress. In many sports, the foot absorbs tremendous shearing and loading forces, sometimes reaching over 20 times the person's body weight. Physicians who treat these disorders must have a good understanding of the anatomy and kinesiology of the foot.

See the following images.

Select bones of the foot (dorsal and plantar views). Select bones of the foot (superolateral view).

Although foot injuries can occur from a variety of causes, the most common cause is trauma. Other etiologies include (1) rapid or improper warm-up, (2) overuse, (3) intense workouts, (4) improper footwear, and (5) playing on hard surfaces.[1, 2, 3, 4, 5]

Physicians who evaluate and treat common foot problems should have a working knowledge of the individual sports and the injuries that are commonly associated with them. An understanding of the basic treatment approaches for these injuries also is imperative.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education articles Broken Foot and Broken Toe.

NextEpidemiologyFrequencyUnited States

Estimates indicate that 15% of sports-related injuries affect the foot alone.

PreviousNextFunctional AnatomyFoot and ankle

The foot is composed of 26 major bones, which can be divided into 3 regions: the forefoot, midfoot, and hindfoot. The forefoot is comprised of the 5 metatarsals and the 14 phalanges. The 3 cuneiforms (ie, lateral, intermediate, medial), the cuboid, and the navicular represent the midfoot. The hindfoot is composed of the talus and the calcaneus (see image below).

The hindfoot is composed of the talus and the calcaneus. The talus is oriented to transmit forces from the foot through the ankle to the leg.The calcaneus is the largest bone in the foot. The Achilles tendon inserts on the posterior aspect of the calcaneus.The navicular lies anterior to the talus and medial to the cuboid.The cuboid articulates with the calcaneus proximally, with the fourth and fifth metatarsals distally, and with the lateral cuneiform medially (see image below). Select bones of the foot (medial and lateral views). Each of the cuneiform bones is wedge-shaped. The medial, intermediate, and lateral cuneiform bones articulate with the first 3 metatarsals distally and the navicular proximally. The cuboid articulates with the lateral cuneiform. The 5 metatarsals articulate with the proximal phalanges.The great toe is composed of 2 phalanges, with 3 for each lesser toe.Although variation exists in the number and location of the sesamoid bones, 2 constant sesamoids are present beneath the metatarsal head. The sesamoids are usually present within tendons juxtaposed to articulations.

Select tendons of the foot (see image below)

Select tendons of the foot. The flexor hallucis longus (FHL) tendon is 1 of 3 structures that lie in the tarsal tunnel. Running behind the medial malleolus, the FHL is the most posterolateral. The FHL runs anterior to insert onto the distal phalanx of the great toe. The FHL acts as a flexor of the great toe, elevates the arch, and assists with plantar flexion of the ankle. The flexor digitorum longus (FDL) tendon passes between the FHL and tibialis posterior tendon. The FDL inserts onto the distal phalanges of the 4 lateral digits and acts to flex the distal phalanges. The tibialis posterior tendon is the most anteromedial of the tarsal tunnel tendons. This tendon inserts on the navicular tuberosity; the 3 cuneiforms; the cuboid; and the second, third, and fourth metatarsals. The tibialis posterior muscle flexes, inverts, and adducts the foot. Laterally, the peroneus longus and peroneus brevis tendons share the common peroneal tunnel running behind and around the lateral malleolus. The peroneus longus plantar flexes the first metatarsal, flexes the ankle, and abducts the foot. The peroneus brevis flexes the ankle and everts the foot. Other important structuresThe plantar aponeurosis or fascia is a deep span of connective tissue extending from the anteromedial tubercle of the calcaneus to the proximal phalanges of each of the toes. Medial and lateral fibrous septa originate from the medial and lateral borders to attach to the first and fifth metatarsal bones. Nerve innervation of the foot runs along the medial and lateral metatarsals and phalanges in a neurovascular bundle. These nerves are vulnerable to compressive forces that, in time, can generate the painful Morton neuroma, which most commonly affects the interspace between the third and fourth metatarsals. Four nerves supply the forefoot: the sural nerve (most lateral), branches of the superficial peroneal nerve, the deep peroneal nerve, and the saphenous nerve. The joint between the forefoot and the midfoot, the tarsometatarsal (TMT) joint or Lisfranc joint, is formed by a mortise of the cuneiform bones surrounding the base of the second metatarsal. This joint is supported by the transverse ligaments, and the Lisfranc ligament joins the medial cuneiform and the base of the second metatarsal. Disruption of this ligament can result in a destabilization of the TMT joint complex of the foot, the result of which can be instability of the arch and the midfoot. PreviousNextSport-Specific Biomechanics

The 3 planes in which the foot and ankle function are the transverse, sagittal, and frontal. Movement is possible in all 3 planes.

Plantar flexion and dorsiflexion occur in the sagittal plane. Plantar flexion involves the foot moving from the anterior leg distally. Dorsiflexion is the opposite motion. Inversion and eversion occur in the frontal plane of motion. Eversion occurs when the bottom of the foot turns away from the midline of the body. Inversion is the opposite action. The 2 transverse plane motions are abduction and adduction. Adduction involves the foot moving toward the midline of the body, whereas abduction is the opposite action. PreviousProceed to Clinical Presentation , Athletic Foot Injuries

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Calcaneofibular Ligament Injury

Background

Ankle injuries are among the most common injuries that present to physician offices and emergency departments (EDs) because the ankle is the most frequently injured joint in the body.[1, 2, 3, 4, 5, 6, 7, 8] Ankle injuries are a major cause of time loss from work or other daily activities and constitute up to 25% of all time-loss injuries from running and jumping sports.[9, 10] Sprains account for 85% of ankle injuries and, of these sprains, 85% are caused by inversion injuries. An inversion sprain results in an injury to the lateral ligaments, one of which is the calcaneofibular ligament (CFL). Most ankle sprains can be managed with a short period of immobilization followed by rehabilitation therapy, but chronic instability is best treated surgically.[11]

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education articles Ankle Sprain and Sprains and Strains.

NextEpidemiologyFrequencyUnited States

An estimated 1 ankle inversion injury occurs per 10,000 people per day, or 23,000 ankle inversion injuries per day. Of these ankle inversion injuries, the CFL is the second most common ligament injured after the anterior talofibular ligament (ATFL).

PreviousNextFunctional Anatomy

The CFL courses from the distal fibula to the calcaneus by extending from the distal anterior margin of the lateral malleolus to insert onto the posterior lateral tubercle of the lateral wall of the calcaneus.[8, 12, 13] The CFL lies deep to the peroneal tendons, is cylindrical in shape, and, because it crosses 2 joints, it acts as a subtalar joint stabilizer.

PreviousNextSport-Specific Biomechanics

The CFL is 20-30 mm long, 3-5 mm thick, and 4-8 mm wide, and the angle of the CFL from the fibula to the calcaneus is 10 º -45 º posterior to the axis of the fibula. Except in the extremes of inversion, the CFL is in a lax position. With an inverted ankle, strain on the CFL is highest in dorsiflexion; thus, when the ankle is dorsiflexed or in a neutral position, the CFL is the lateral ligament that is most often injured in inversion sprains. Although isolated CFL tears are uncommon, CFL tears in combination with ATFL tears are the second most common injury pattern (20% of injuries). Midsubstance rupture of the CFL remains the most common injury pattern, although a number of fibula or calcaneus avulsion-type injury patterns exist.[14]

PreviousProceed to Clinical Presentation , Calcaneofibular Ligament Injury

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Talofibular Ligament Injury

Background

Ligamentous injuries of the ankle are common among athletes.[1, 2] Inversion injuries of the ankle account for 40% of all athletic injuries. The anterior talofibular ligament (ATFL) and the calcaneofibular ligament (CFL) are sequentially the most commonly injured ligaments when a plantar-flexed foot is forcefully inverted. The posterior talofibular ligament (PTFL) is rarely injured, except in association with a complete dislocation of the talus.[3, 4, 5]

Ligamentous injuries of the ankle are classified into the following 3 categories, depending on the extent of damage to the ligaments:[6, 7, 8, 9, 10]

Grade I is an injury without macroscopic tears. No mechanical instability is noted. Pain and tenderness is minimal.Grade II is a partial tear. Moderate pain and tenderness is present. Mild to moderate joint instability may be present.Grade III is a complete tear. Severe pain and tenderness, inability to bear weight, and significant joint instability are noted.

For excellent patient education resources, visit eMedicineHealth's First Aid and Injuries Center. Also, see eMedicineHealth's patient education articles Ankle Sprain and Sprains and Strains.

Related Medscape Reference topics:

Ankle Impingement Syndrome

Ankle Sprain

Ankle Taping and Bracing

Related Medscape resources

Resource Center Exercise and Sports Medicine

Resource Center Joint Disorders

Specialty Site Orthopaedics

NextEpidemiologyFrequencyUnited States

Approximately 3600 cases of talofibular ligament injury per 100,000 people are reported per year.

PreviousNextFunctional Anatomy

The lateral articular capsule of the ankle can be divided into anterior and posterior segments. The anterior segment attaches proximally to the anterior portion of the distal tibia superior to the articular surface and to the border of the articular surface of the medial malleolus. The posterior segment attaches distally to the talus just posterior to its superior articular facet and attaches laterally to the depression in the medial surface of the lateral malleolus.[3, 4, 5]

The ATFL is intracapsular and attaches anteriorly to the anterior border of the distal fibula and laterally to the neck of the talus. The PTFL attaches posteriorly to the digital fossa of the fibula and laterally to the lateral tubercle on the posterior portion of the talus.

PreviousNextSport-Specific Biomechanics

The talofibular ligaments along with the CFL are components of the lateral ligament complex. This complex becomes stressed when the ankle is inverted and plantar flexed.[11] Supination of the foot in neutral flexion usually results in injury of the CFL. Supination and adduction injuries tear both the ATFL and the CFL.

The PTFL is the strongest of the lateral ligaments, and extreme inversion with plantar flexion is required to place the PTFL under stress; as a result, the PTFL is less commonly injured.[11] Transient subluxation or dislocation of the talus from the tibial mortise usually results in injury of all 3 lateral ligaments. Prevention of anterior displacement of the talus is primarily a function of the ATFL. Little additional motion occurs when the CFL also is damaged. Instability to inversion is greater when both the CFL and the ATFL are injured than when either ligament is injured alone.

PreviousProceed to Clinical Presentation , Talofibular Ligament Injury

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Femoral Neck Fracture

Background

The number of individuals participating in athletic activities is continually increasing, whether these individuals are highly competitive athletes or weekend sports enthusiasts.[1, 2] Stress fractures of the femoral neck are uncommon injuries (see image depicted below). In general, these injuries occur in 2 distinct populations, (1) young, active individuals with unaccustomed strenuous activity or changes in activity, such as runners or endurance athletes, and (2) elderly individuals with osteoporosis.[3] Elderly individuals may also sustain femoral neck stress fractures; however, hip fractures are much more common and are often devastating injuries.

Classification of femoral neck stress fractures.

Femoral neck fractures in young patients are usually caused by high-energy trauma. These fractures are often associated with multiple injuries and high rates of avascular necrosis and nonunion. Results of this injury depend on (1) the extent of injury (ie, amount of displacement, amount of comminution, whether circulation has been disturbed), (2) the adequacy of the reduction, and (3) the adequacy of fixation. Recognition of the disabling complications of femoral neck fractures requires meticulous attention to detail in their management.

For excellent patient education resources, see eMedicineHealth's patient education article Total Hip Replacement.

NextEpidemiologyFrequencyUnited States

Stress fractures of the femoral neck are uncommon, but they may have serious consequences. Markey reported that femoral neck fractures comprise 5-10% of all stress fractures. Certain groups of athletes, including long-distance runners who suddenly change or add activities, appear to have a higher prevalence of femoral neck stress fractures compared with the general population.

Plancher and Donshik reported a prevalence rate of at least 10% for ipsilateral femoral shaft fractures, of which 30% are missed on the initial presentation.[4] Brukner reported that women have a higher rate of stress fractures than men, with relative risks ranging from 1.2 to 10 for similar training volumes.[5] Training errors are the most common risk factors, including a sudden increase in the quantity or intensity of training and the introduction of a new activity.

A number of factors predispose the elderly population to fractures, including osteoporosis, malnutrition, decreased physical activity, impaired vision, neurologic disease, poor balance, and muscle atrophy. Hip fractures are common and are often devastating in the geriatric population.[6] More than 250,000 hip fractures occur in the United States each year; however, as reported by Koval and Zuckerman, with an aging population, the annual number of hip fractures is expected to double by the year 2050.[7]

Prevention of osteoporosis is key to reducing these numbers, as osteoporosis remains the single most important contributing factor to hip fractures. The prevalence of hip fractures, regardless of location, is highest among white women, followed by white men, black women, and black men.

Koval and Zuckerman noted the age-adjusted incidence of femoral neck fractures in the United States is 63.3 cases per 100,000 person-years for women and 27.7 cases per 100,000 person-years for men.[7] Femoral neck fractures in elderly patients occur most commonly after minor falls or twisting injuries, and they are more common in women. In addition, Joshi et al noted stress fractures of the ipsilateral femoral neck as a rare consequence of total knee arthroplasty.[8] Influencing factors are correction of a significant knee deformity and inactivity before the total knee arthroplasty.

International

The exact incidence of femoral neck stress fractures is not known. Volpin et al reported a rate of 4.7% in 194 Israeli military recruits.[9] Zahger et al reported a higher rate of femoral neck stress fractures in Israeli female military recruits.[10] Insufficiency fractures are more common in females secondary to osteoporosis.

PreviousNextFunctional Anatomy

The femoral aspect of the hip is made up of the femoral head with its articular cartilage and the femoral neck, which connects the head to the shaft in the region of the lesser and greater trochanters. The synovial membrane incorporates the entire femoral head and the anterior neck, but only the proximal half of the posterior neck. The shape and size of the femoral neck vary widely.

Crock standardized the nomenclature of the vessels around the base of the femoral neck. The blood supply to the proximal end of the femur is divided into 3 major groups. The first is the extracapsular arterial ring located at the base of the femoral neck. The second is the ascending cervical branches of the arterial ring on the surface of the femoral neck. The third is the arteries of the ligamentum teres.

A large branch of the medial femoral circumflex artery forms the extracapsular arterial ring posteriorly and anteriorly by a branch from the lateral femoral circumflex artery (see images shown below). The ascending cervical branches ascend on the surface on the femoral neck anteriorly along the intertrochanteric line. Posteriorly, the cervical branches run under the synovial reflection toward the rim of the articular cartilage, which demarcates the femoral neck from its head. The lateral vessels are the most vulnerable to injury in femoral neck fractures.

Posterior view of the extraosseous blood supply to the femoral head. Anterior view of the extraosseous blood supply to the femoral head.

A second ring of vessels is formed as the ascending cervical vessels approach the articular margin of the femoral head. From this second ring of vessels, the epiphyseal arteries are formed. The lateral epiphyseal arterial group supplies the lateral weight-bearing portion of the femoral head. The epiphyseal vessels are joined by the inferior metaphyseal vessels and vessels from the ligamentum teres.

Femoral neck fractures frequently disrupt the blood supply to the femoral head (see images below). The superior retinacular and lateral epiphyseal vessels are the most important sources of this blood supply. Widely displaced intracapsular hip fractures tear the synovium and the surrounding vessels. The progressive disruption of the blood supply can lead to serious clinical conditions and complications, including osteonecrosis and nonunion.

Posterior view of the extraosseous blood supply to the femoral head. Anterior view of the extraosseous blood supply to the femoral head.

In 1961, Garden described the classification of femoral neck fractures. In this classification, femoral neck fractures are divided into the following 4 grades based on the degree of displacement of the fracture fragment:

Grade I is an incomplete or valgus impacted fracture.Grade II is a complete fracture without bone displacement.Grade III is a complete fracture with partial displacement of the fracture fragments.Grade IV is a complete fracture with total displacement of the fracture fragments.

Frandersen et al concluded that clinically differentiating the 4 grades of fractures is difficult. Multiple observers were able to completely agree on the Garden classification in only 22% of the cases. Hence, classifying femoral neck fractures as nondisplaced (Garden grades I or II) or displaced (Garden grades III or IV) is more accurate. See the illustration depicted below.

Garden fracture classification.

Femoral neck fractures are usually intracapsular. The femoral neck has essentially no periosteal layer; hence, all healing is endosteal in origin. The synovial fluid bathing the fracture may interfere with the healing process. Angiogenic-inhibiting factors in synovial fluid can inhibit fracture repair. These factors, along with the precarious blood supply to the femoral head, make healing unpredictable and nonunions fairly frequent.

Bone physiology

Bone is a dynamic tissue, which continually reacts to stressful events. According to data from Maitra and Johnson, stress fractures result from an imbalance between bone resorption and bone deposition during the host bone response to repeated stressful events.[11] Most cortical stress involves tension or torsion; however, bone is weaker in tension and tends to fail by fracturing along a cement line.

Maitra and Johnson went on to report that tension forces promote osteoclastic resorption, whereas compressive forces promote an osteoblastic response.[11] With repeated stress, new bone formation cannot keep pace with bone resorption. This inability to keep up results in thinning and weakening of cortical bone, with propagation of cracks through cement lines, and, eventually, the development of microfractures. Without proper rest to correct this imbalance, these microfractures can progress to clinical fractures, the sine qua non of overuse.

A stress fracture is the result of a dynamic process over time, unlike an acute fracture, which is usually the result of a single supraphysiologic event. Markey reported that stress fractures can be described as a normal host response to abnormal stress, and this is different from insufficiency fractures, which are an abnormal host response to normal stresses.[12]

Devas, in 1965, classified stress fractures into 2 types that differ radiologically and have different clinical outcomes.[13] The first is the tension stress fracture, which results in a transverse fracture directed perpendicular to the line of force transmitted in the femoral neck and originates at the superior surface of the femoral neck. This fracture pattern is at increased risk for displacement. These fractures carry a risk for further advancement of the fracture line superiorly and eventual displacement, leading to nonunion and avascular necrosis. Hence, early diagnosis and treatment are essential.

The second type is a compression type of femoral neck stress fracture, which has evidence of internal callus formation on radiographic images. The fracture is usually located at the inferior margin of the femoral neck without cortical discontinuity. This fracture pattern is thought to be mechanically stable. The compression fracture occurs mostly in younger patients, and continued stress does not usually cause displacement. The earliest radiographic evidence of a compression stress fracture is usually a haze of internal callus in the inferior cortex of the femoral neck. Eventually, a small fracture line appears in this area, and it gradually scleroses.

Fullerton and Snowdy described a femoral neck stress fracture classification with the following 3 categories[14] : (1) tension, (2) compression, and (3) displaced, as depicted below. Tension fractures occur on the superolateral aspect of femoral neck and are at high risk for displacement. Compression fractures are similar to those described by Devas, which occur on the inferomedial aspect of the femoral neck and have a low risk for displacement.

Classification of femoral neck stress fractures. PreviousNextSport-Specific Biomechanics

Several theories have been developed to explain the mechanisms of femoral neck stress fractures and the biomechanics of the hip. Nordin and Frankel described the biomechanics of the hip. The load on the femoral neck can exceed 3-5 times the body weight when an individual is walking or running. Gravity acts on the center of the body mass, which results in torque on the medial aspect of the hip joint. This torque is counterbalanced by the contraction of the gluteus medius and minor. The total load on the femoral head is the sum of the forces producing these 2 torque forces. Then, these forces on the femoral head are transmitted through the femoral neck to the shaft, which create a significant amount of stress on the femoral neck as a result of compression and bending.

Minimal tension or compressive strains have been confirmed to occur in the superior aspect of the femoral neck during a normal single-leg stance. When tension increases, the inferior aspect of the femoral neck takes over the burden of damping the forces of compression. When a patient bends forward, stress is induced on the superior aspect of the femoral head; however, counter traction of the abductor muscles also occurs. Hence, if the gluteus medius muscle is fatigued, the strain is placed entirely on the superior aspect of the femoral neck. This strain can predispose patients to femoral neck stress fractures. If the abductor muscles fatigue and are unable to provide normal tension, the tensile stress in the femoral neck increases.

Muscle fatigue has been implicated as a contributing factor in the development of stress fractures. Muscle imbalance leads to changes in the application of stress across the femoral neck that may exceed the bone's capability to respond appropriately to stress. Muscle fatigue secondary to repetitive activity can decrease its shock-absorbing capacity so that higher peak stresses occur in the femoral neck. This can lead to gait abnormalities, which, in turn, can alter the body's center of gravity and change the patterns of stress placed on the femoral neck.

In the 1960s, Frankel proposed that femoral neck fractures occur in the presence of a high ratio of axial load to bending load. Altered muscle balance may also increase the risk of a hip fracture. Another theory is that a fall onto the hip with a direct blow to the greater trochanter may generate an axial force along the neck, creating an impaction fracture. The combination of axial and rotational forces has also been proposed as a mechanism.

The miserable malalignment syndrome combines femoral neck anteversion, genu valgum, increased Q-angle, tibia vera, and compensatory foot pronation that may not allow individuals to compensate for overuse. Leg-length discrepancy may also predispose individuals to injuries by creating an unequal distribution of stress and tension across the hip joint.

PreviousProceed to Clinical Presentation , Femoral Neck Fracture

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Groin Injury

Introduction and Frequency

Groin injuries are commonly encountered by physicians and clinicians who treat athletes of all ages at all levels of competition. Groin injuries are particularly common in activities in which forceful adduction of the hip occurs; examples include skating, ice hockey, swimming, and soccer. In fact, as many as 10% of ice hockey–related injuries and 5% of soccer-related injuries are groin injuries.[1, 2] This article focuses on acute and chronic groin injuries related to sporting activities. Groin injuries resulting from major trauma (eg, multiple trauma, penetrating injuries) are not addressed, except to note that they require emergent medical evaluation.

The images shown below illustrate the relevant anatomy of the pelvis relating to groin injuries.

Pelvis, symphyseal aspect. Pelvis, frontal view. Pelvis, lateral aspect.

Give special consideration to children, adolescents, and females with groin pain, because these conditions in this patient population may be erroneously attributed to minor trauma when they are, in fact, serious and require medical or surgical intervention. Evaluate any child aged 2-15 years with groin pain and an antalgic gait, especially if he or she has a fever. Avascular necrosis (AVN) of the hip, Legg-Calve-Perthes disease, septic arthritis, and slipped capital femoral epiphysis must be ruled out.[3] Consider early orthopedic consultation in any such case.

Hip pain in the adolescent athlete must take into consideration the relatively weaker growth plate of certain bony structures in the hip, and it should prompt the clinician to consider the diagnosis of apophyseal avulsion fractures. Apophysitis and apophyseal fractures are more common in skeletally immature athletes, in whom the physis is the weakest link in the muscle – tendon – bone complex.[4] Moreover, remember that children and adolescents may report knee pain that is actually referred from pathology in the hip, or vice versa. That is, complaints of both hip and lower-extremity pain in children and adolescents merit a detailed physical examination of the affected joint and surrounding structures.

The initial evaluation and conservative treatment for adult female athletes may be similar to that of male athletes. However, epidemiologic findings suggest that differences in female body mechanics may lead to subtly different injury patterns and a need for specialized rehabilitation services.[5] Although anatomic differences are obvious, several factors play important roles in determining injury patterns in female athletes. These factors include (1) differences in metabolism, circulation, and cardiorespiratory capacity; and (2) differences in body shape, size, and composition. An example of such is the higher rate of patellofemoral disorders in female athletes, possibly accounted for by an increased quadriceps angle, less developed vastus medialis, and greater degree of genu valgum.[6]

For patient education resources, see the Sports Injury Center, as well as Muscle Strain and Hernia.

Go to Female Athlete Triad, Low Energy Availability in the Female Athlete, and Osteitis Pubis for complete information on these topics.

NextFunctional Anatomy and Sport-Specific Biomechanics

See the following images, which illustrate the relevant anatomy.

Pelvis, symphyseal aspect. Pelvis, frontal view. Pelvis, lateral aspect. Thoracoabdominal and proximal lower-extremity musculature.

The hip joint is formed by the femoral head and its articulation with the acetabulum. The femoral neck and its bony prominences, the greater trochanter laterally and the lesser trochanter medially, are the attachment points for the major muscle groups of the hip. The abductor muscles of the hip, the gluteus medius and minimus, and the external rotators of the hip attach to the greater trochanter; the gluteus maximus, the main extensor of the hip joint, along with the hamstrings, attaches to the femur just distal to the greater trochanter. The lesser trochanter is the site of attachment for the iliopsoas muscle, the major hip flexor.[7]

The main blood supply to the femoral head and neck is the medial femoral circumflex artery, a branch of the common femoral artery. Disruption of the blood supply, through direct trauma (fractures of the femoral neck) or through vaso-occlusive disorders (sickle cell crisis), is related to the development of avascular necrosis of the femoral head.

There are approximately 18 bursae located throughout the hip joint. The superficial bursa located over the greater trochanter is a common source of pain as a result of inflammation; the deep bursa, or the gluteus medius bursa, is another common source of hip pain. The deep bursa lies between the gluteus maximus tendon and the posterolateral prominence of the greater trochanter.[7]

The hip is the largest joint in the body. The range of motion of the hip joint is impressive, second only to that of the shoulder joint. This factor, combined with the fact that the hip joint bears weight and is subjected to repetitive stress, makes this joint extremely susceptible to injury. In an Australian study of 29 elite soccer players, Verrall et al suggested that the development of chronic groin injury may be preceded by hip stiffness—that a restricted range of motion of the hip may in fact be a risk factor for this condition.[8] Even minor groin injuries can be difficult to rehabilitate.

Most groin injuries are related to stress and strain on the hip joint and the surrounding bony and muscular support structures of the pelvis. The most common injuries can be divided into acute and chronic injuries. The most common acute injuries are soft-tissue contusions and hematomas that result from direct force. The most common chronic conditions are strains of the muscle–tendon unit.[9]

Acute groin injuries may result from direct trauma encountered in contact sports (eg, football, ice hockey, basketball, rugby, soccer) and noncontact sports (eg, gymnastics). Acute muscle strains are commonly encountered in activities in which forced adduction of the hip occurs (eg, soccer, football, rugby, ice hockey, swimming [particularly with the breaststroke]) or in activities in which forced abduction of the hip occurs (eg, any sporting activity in which the athlete may perform a split, either accidentally or forcefully).

The causes of acute groin injuries may be considered causes of chronic (overuse) injuries. Chronic groin injuries tend to occur in those who participate in activities that promote overuse of the groin area (eg, swimming [particularly the breaststroke], ice hockey, speed and figure skating, soccer, running).

Go to Hip Pointer, Hip Tendonitis and Bursitis and Pediatrics, Sickle Cell Disease for complete information on these topics.

PreviousNextApproach to History Taking and Physical Examination

The approach to the athlete with groin pain can challenge the clinician for a variety of reasons.[10] The description and location of the pain is often vague. The anatomy of the groin can be clinically difficult to define.

The groin consists of the area where the abdomen meets the legs and includes the structures of the perineum. The groin, therefore, includes the following: the lower rectus abdominis musculature, the inguinal region, the symphysis pubis, the upper portions of the adductor muscles of the thigh, and the genitalia, as well as the scrotum in males.

The history and physical examination should be approached systematically to avoid missing the diagnosis. The clinician should assess for the onset of pain and whether the athlete can recall the inciting event, if any. The clinician should discuss factors that aggravate and alleviate pain, especially those pertinent to the sport in which the athlete participates.

The physical assessment requires the exposure of as much of the groin and hip as permitted, and the examination must include the following: inspection for symmetry and anatomic irregularity; palpation of the affected area for deformity; assessment of the range of motion of the articular structures near the area; rotation of the hip joint; observation for discrepancy of leg length; and evaluation of the patient's gait, including the performance of sprints, jumps, and activities that exacerbate the athlete's pain.

The differential diagnosis must take into consideration a number of medical conditions that affect the groin region in all individuals, not solely athletes.[4] These include the following:

Intra-abdominal disorders – Appendicitis, inflammatory bowel diseaseGenitourinary abnormalities – Urinary tract infections; sexually transmitted diseases; gynecologic, scrotal, and testicular abnormalities; nephrolithiasisReferred lumbosacral pain from lumbar disc diseaseHip joint disorders – Osteoarthritis, Legg–Calve–Perthes disease, synovitis, slipped capital femoral epiphysis, osteochondritis desiccans

Because an estimated 27-90% of patients with groin pain have more than one coexisting injury, it is possible for clinicians to diagnose and manage one injury while a second injury goes unrecognized and untreated.[4, 11] The importance of a wide differential diagnosis is clearly evident from such a statistic.

The specific historical and physical examination findings germane to specific groin injuries will be discussed in the sections that follow. The patterns of pain described by patients, however, suggest types of pathologic processes at and around the hip joint. Pain that is aggravated by use and alleviated with rest suggests a structural problem, such as that encountered with osteoarthritis. Constant pain suggests an infectious, inflammatory, or neoplastic process.[7]

Go to Urinary Tract Infection in Females and Urinary Tract Infection in Males for complete information on these topics.

PreviousNextClinically Encountered Groin InjuriesImpact injuries

Impact injuries, such as those that occur during football, hockey, or other contact sports that produce high-speed collisions, usually result in contusions. However, such injuries may cause fractures of the pelvis (iliac wing); they may exacerbate previously asymptomatic inguinal hernias; and, in rare cases, they may produce bladder, testicular, or even urethral (straddle) injuries.

Any patient with lower abdominal or pelvic impact injury that causes severe groin pain, loss of function, or blood in the urine should be immediately evaluated by a physician. Findings from anteroposterior radiographs of the pelvis, hip images, and dipstick urinalysis are usually sufficient to rule out a serious acute injury. If no bony injury is discovered, conservative measures, namely, rest, application of ice for the first 24-48 hours, compression, and nonsteroidal anti-inflammatory drugs (NSAIDs), may be implemented. A urologist should also evaluate the patient for hematuria.

Hip pointer

The hip pointer encompasses both impact and strain injuries of the hip. Forced extension of the hip may result in a sprain or avulsion of the sartorius muscle at its attachment to the iliac crest. These injuries are severely painful and difficult to rehabilitate. Contusions to the anterior superior iliac crest may involve the attachment of the sartorius muscle as well as the lateral femoral cutaneous nerve, causing pain and paresthesias to radiate down the lateral aspect of the thigh. In some of these cases, especially those in which trochanteric bursitis is suspected, a local anesthetic or steroid injections may be given (at the physician's discretion) to treat severe pain.[12]

Groin pull

Acute strain injuries of the groin are epitomized by the groin pull. Multiple muscles, including the iliopsoas muscle, the adductor group, and the gracilis muscle, attach to the medial portion of the femur or pubis and help keep the legs together and flex the thigh. Falling, running, and quickly changing directions, as well as kicking or doing the splits (either intentionally or otherwise) can result in these injuries. Groin pulls can cause pain in the groin that radiates down the inside of the thigh.

The injury is usually focused at the musculotendinous junction and involves disruption of the fibers to various degrees and, occasionally, hematoma formation, which may delay healing. These weakened areas are repaired by fibroblasts, but they continue to be susceptible to repeat injury for a long time.[5] In fact, in a review of 1292 National Hockey League players, those with a previous groin injury had twice the risk of repeat injuries as that of athletes without a previous injury.[13] Furthermore, veteran hockey players had an injury rate 5 times greater than that of rookie players.[13]

In another review, the National Hockey League statistics revealed that adductor strains occurred 20 times more frequently during training camp than during the regular season, possibly related to the benefits of a strength-training program and to the fact that off-season deconditioning may contribute to these injuries.[4]

Sometimes, the relevant muscles may actually tear loose from their bony attachments, taking a piece of the bone with it. If these avulsion fractures are severely displaced, surgical repair may be required. Most groin pulls eventually respond to conservative treatment that consists of rest, the application of ice, compression, and the use of NSAIDs. These injuries may be adequately managed by the team physician or trainer.

Injuries of the muscle–tendon units

Several muscle–tendon units are commonly strained and injured in athletes. The muscle most commonly strained and injured in the abdomen and groin is the adductor longus muscle.[9] Other muscle–tendon units that must be considered include the rectus femoris, the rectus abdominis, the sartorius, the gracilis, and the iliopsoas.

The rectus abdominis strain is an injury that may cause acute or chronic groin pain. This strain results from injury to the rectus muscle of the abdominal wall, which attaches to the pubis. This injury is fairly common in skaters, hockey players, and swimmers (especially breaststrokers). Severe tears and sprains of the rectus muscle are slow to recover; they may result in significant hematoma formation; and, on rare occasions, they may require surgical repair or reinforcement.[14]

Strain of the adductor longus may be managed in a variety of ways, depending on the location of the injury. Physical examination may reveal whether the injury lies within the muscle belly or within the tenoperiosteal attachment. Injuries to the muscle belly are best managed with gentle stretching, strengthening, and liberal return to activity. Injuries to the tenoperiosteal attachment require more conservative management: rest until the patient is pain free; gentle stretching and strengthening over a period of weeks; running and sprinting; and, lastly, running and sprinting combined with rapid changes in direction.[15]

Hernias

Hernias of the abdominal wall must be considered in patients who present with abdominal or groin pain. Hernia pain can be confused with pain due to chronic conditions encountered in a variety of sporting activities. Therefore, hernias represent a pathologic process that is frequently overlooked in the athlete. In fact, only 8% of patients with abdominal or inguinal hernias had detectible hernias on physical examination.[9] Therefore, a high index of suspicion is recommended when evaluating patients with groin or abdominal pain, and a hernia must be considered in the differential diagnosis. Herniography depicts a disorder in 84% of patients, and more importantly, 50% of these patients with abdominal wall defects do not have pain.[9]

Treatment for hernias is conservative and includes rest; the application of ice; gentle range-of-motion exercises; and, ultimately, surgical repair with mesh reinforcement of the abdominal wall (in more serious conditions). In comparing the recovery times for patients after hernia repair, Stoker and colleagues cited differences when open surgical repair was compared with laparoscopic repair. The authors suggested that full recovery may require as long as 2-3 weeks in patients with open surgical repair, whereas patients who undergo laparoscopic repair are more likely to resume participation in 1 week.[16]

Sportsman's hernia

The sportsman's hernia, or Gilmore groin, was first described by O.J. Gilmore in 1980.[17] It is a syndrome characterized by chronic groin pain that is associated with a dilated superficial inguinal ring, although the exact cause of this injury is largely speculative and likely multifactorial.[4] The true incidence of sportsman's hernia remains controversial; some authors believe it is only a rare cause of groin pain in athletes, but others believe it is the most common cause of chronic groin pain.[4]

The term "sportsman's hernia" is a misnomer, however, as there is typically no demonstrable hernia or defect in the groin or the abdominal wall. The definition of the sportsman's hernia, therefore, is any condition that causes persistent unilateral pain in the groin without a demonstrable hernia.[18]

The classic operative findings include laddering of the external oblique in conjunction with separation of the conjoint tendon from the ligament and laxity of the transversalis fascia.[19] Other studies have suggested abnormalities with the rectus abdominis insertion, avulsions of the internal oblique muscle fibers at the pubic tubercle, or entrapment of the ilioinguinal or genitofemoral nerves.[20]

Historically, the pain is described as chronic, located near the pubic tubercle, maximal on the evening of vigorous exercise or on the morning afterward, and exacerbated by activities that increase the intra-abdominal pressure. It is believed that sportsman's hernias are the result of chronic, repetitive trauma or stress to the musculotendinous portions of the groin, the pain of which develops insidiously, rather than acutely or dramatically. The sportsman's hernia is more commonly encountered in male than female athletes, and predictors of the development of groin injuries observed in professional hockey players included previous injury, nonaggressive conditioning in the off-season, and veteran, or older, players.[18]

On digital examination, the superficial inguinal ring is dilated. Evidence of herniation may or may not be palpable. The point of most tenderness is often the ipsilateral pubic tubercle. Pain can be elicited with a Valsalva maneuver or a resisted sit-up. Examination of the hip joint and evaluation of the athlete's gait typically reveal weakness with adduction.

Conservative therapies may temporarily alleviate the patient's pain, but definitive surgical management is recommended. Over 9 years, Gilmore repaired 360 injuries with a technique that used 6-layered reinforcement of the weakened transversalis fascia. Approximately 97% of his patients returned to competitive sports by the 10th week after postoperative care.[19] When conservative therapy does not result in alleviation of symptoms, surgical exploration is indicated, and placement of prosthetic meshes or patches, with or without neurectomy or ablation of the ilioinguinal nerve, has demonstrated success.[18]

Hip fracture or dislocation

The most severe and potentially debilitating groin injury is the hip fracture or dislocation. This injury normally results from a violent or high-speed collision or fall, for example, in skiing or playing hockey. The pain is usually severe and associated with an inability to bear weight and with a shortening and rotation of one leg inward or outward. Other severe injuries may be associated with the amount of force required to fracture or dislocate a hip. Immobilization and immediate medical attention and reduction (within the first few hours) are required to maximize the potential for recovery.

Stress fractures

Stress fractures of the femoral neck and the pubic ramus are the 2 most common stress fractures of the groin region.[21] Stress fractures are caused by repetitive minor trauma to the bones or muscular attachments. Therefore, these injuries are categorized somewhere between acute injuries and chronic injuries. Most stress fractures occur secondary to running (eg, in joggers or military recruits), although additional risk factors include relative osteoporosis in young female athletes secondary to nutritional or hormonal imbalances, muscle fatigue, changes in foot gear and training, or changes in intensity and/or duration of training.[21]

Stress fractures in the groin or hip can be difficult to diagnose and treat; these injuries most commonly occur at the femoral neck and inferior pubic ramus.

Femoral neck stress fractures are especially troublesome because they may lead to AVN of the femoral head and long-term disability. These may appear as a cortical irregularity or haziness on plain radiographs, but a magnetic resonance image (MRI) or a bone scan is usually required for the definitive diagnosis. The treatment is conservative, and recovery, although usually complete, may take months, especially if the athlete's activity is not significantly curtailed.

Avulsion fractures

Avulsion fractures of the hip must be considered in young athletes who give a history of severe, sudden-onset, and well-localized pain over a bony prominence. The relative weakness of the apophysis of the adolescent skeleton predisposes the young athlete to a variety of avulsion fractures. Examples include the following: avulsion of the anterior inferior iliac spine due to forceful flexion of the hip by the rectus femoris, avulsion of the ischial tuberosity by the hamstrings, and avulsion of the anterior superior iliac spine caused by the sartorius muscle.

Management for the majority of avulsion fractures is conservative and typically includes rest and gradual return to activity, aided by the use of analgesics.[22] Controversy exists regarding the management of avulsion fractures of the ischial tuberosity. Some authors advocate nonsurgical management. However, others have reported deficits in strength; function; and, in some cases, the formation of a painful callus, which prompts their advocacy of early surgical repair.[5] Depending on the size and amount of displacement of the fracture fragment, the injury may warrant surgical repair; this decision must be left to the judgment of the clinician.

AVN of the femoral head

AVN of the femoral head is a progressively debilitating condition that most often affects individuals in their third or fourth decade of life. An estimated 10,000-20,000 cases occur annually, at a mean age of 34 years. Although the pathogenesis is largely unclear, disruption of the circulatory supply to the femoral head either acutely or chronically results in cell destruction and necrosis, leading to collapse of the bony framework of the joint and resulting in arthritis.[21]

Risk factors for the development of AVN include high loads, sudden or irregular impact, and preexisting abnormalities such as dysplasia of the hip.[23] Tears of the labrum have been associated with developmental dysplasia[21] and early osteoarthritis and AVN.[23]

Ninety percent of cases of nontraumatic AVN are associated with systemic corticosteroid use for the management of asthma, chronic obstructive pulmonary disease, or autoimmune disorders. Heavy alcohol consumption has also been associated with the development of AVN.[21]

The diagnosis of AVN first begins with a high index of suspicion and radiographic confirmation of the lesion. Plain radiography may not demonstrate AVN until 3 months after the initial insult; therefore, MRI is the imaging modality of choice for identifying early AVN. MRI is both sensitive and specific (88-100%).[21]

Management includes rest, restricted weight bearing, and symptom control, although studies have demonstrated discrepancies between conservative management and early surgical core decompression.[21]

Osteitis pubis

Osteitis pubis (gracilis syndrome) is a chronic injury that causes resorption of the bone or cartilage of the pubic symphysis due to repetitive stress from kicking, lifting, running, or jumping. Osteitis pubis manifests as pain and tenderness in the region of the pubic symphysis. This injury is believed to be secondary to shearing and/or rotational movement of the pubic symphysis, and it is usually more severe when it occurs in postpartum women, in whom the injury results from the normal laxity of the pelvic ligaments during pregnancy that may persist for some time after delivery.

The patient's history reveals pain, most commonly during or after kicking. Physical examination reveals tenderness over the symphysis pubis. The pain in osteitis pubis results from limited rotation of the hip that transfers stress by shearing or by distraction across the symphysis and disrupts the joint.

Most cases of osteitis pubis are self-limited, and whether the cessation of activity or continued activity delays recovery is unclear. Most authors recommend continued flexibility training and muscle-strengthening exercises during the recovery phase of the injury. Groin support with neoprene shorts may provide some comfort.

Therapy with analgesics may be recommended. The use of corticosteroids is controversial; because corticosteroids are catabolic, some believe that their use may loosen the symphysis and result in a lack of integrity of the structure.[15] One case series, however, demonstrated a benefit when corticosteroids were used in athletes whose symptoms were 2 weeks or less in duration, whereas athletes whose symptoms lasted greater than 16 weeks required an additional 11-16 weeks for symptomatic improvement.[21]

Recovery usually occurs over 2-3 months because of the relatively poor circulation to the region. Some authors note that the average healing time for osteitis pubis is 9-10 months, although most cases are self-limited.[21]

Bursitis

The last chronic or repetitive stress injury is bursitis. The body has special fluid-filled sacs called bursae, which provide lubrication in needed areas, such as the points where muscles move over bony projections. Bursae can become inflamed and irritated, resulting in pain when the overlying muscle is used. Subtle alterations in gait or gait impairment can increase the friction transmitted to the bursal sac. The result of increased friction is thickening of the normally thin bursa wall, leading to fibrosis and a gradual inability to lubricate the outer hip. Lateral hip pain that is aggravated by direct pressure is the classic pattern associated with trochanteric bursitis.[7]

The treatment is conservative, with most cases responding to NSAIDs and rest or to corticosteroid injections, used at the discretion of a physician. Persistent and recurrent bursitis may be due to rheumatic or arthritic disease or gout, which requires special medical treatment.

Meralgia paresthetica

Lateral hip pain accompanied by paresthesias or hyperesthesia is the presentation of lateral femoral cutaneous syndrome, or meralgia paresthetica. Pain that accompanies this disorder is described as a burning or an uncomfortable, heightened sensation.[7] The localized area of pain or hyperesthesia is not affected by direct pressure, movement of the hip joint, or movement of the lower back.

The lateral femoral cutaneous nerve is a pure sensory nerve whose path from the lumbosacral nerve plexus through the abdominal cavity and into the subcutaneous tissue of the thigh renders it susceptible to compression. The result of this compression is a localized area of hyperesthesia or paresthesia, in contrast to sciatica, a condition in which pain extends over a much wider area and extends down the leg and into the foot.[7]

Femoroacetabular impingement

Femoroacetabular impingement (FAI), or hip impingement, has become an increasingly recognized cause of hip pain in adolescents, adults, and athletes. It is believed to result from abnormal contact stress and joint damage around the hip, most notably from prolonged sitting, leaning forward, getting in and out of a vehicle, or performing a pivoting motion in sports. Clinically, pain may be described as either insidious or acute in onset. The clinical evaluation tool most sensitive for FAI is the flexion, adduction, and internal rotation (FADIR) test and reproduces the patient's pain along the anterolateral hip.[24]

Physiologically, it is believed to result from a bony deformity or spatial malorientation of the femoral head or the head/neck junction, acetabulum, or both.[25]

Evidence demonstrates that FAI may initiate osteoarthritis of the hip. Plain radiographic evaluation of the hip (anteroposterior pelvis and frog-leg lateral radiographs) may demonstrate pincer-type FAI, cam lesions, and osteophytes on the anterior femoral neck.[24] Arthroscopic evaluation demonstrates labral tears and acetabular cartilage lesions. It is believed that clinical and radiographic characteristics--namely, male sex, older age, Tonnis osteoarthritis grade, and elevated alpha angle--are associated with more severe intra-articular hip disease observed on arthroscopic evaluation, suggesting these characteristics may serve a predictive function in the evaluation of FAI.[26] Patients with more severe osteoarthritic changes demonstrated radiographically and patients with more severe cartilage damage observed intraoperatively are believed to have worse outcomes with treatment for FAI.[27]

Currently the mainstays of nonoperative treatment for FAI include occupational and physical therapy, restriction of activities that cause pain, core strengthening, and nonsteroidal anti-inflammatory drugs. Surgical treatment, including surgical dislocation of the hip, arthroscopy, periacetabular and rotational osteotomies, and combined hip arthroscopy with limited open exposure, may be necessary to allow full return to activity. There is, however, no long-term prospective data to determine which therapeutic modality offers the most definitive result.[28]

Other injuries

Injuries to the groin that do not involve the bones or musculature are usually the result of a direct impact. All of the soft-tissue structures of the groin are susceptible to these types of injury. Injury to the genitalia (eg, penis, testis, urethra) or bladder, or traumatic inguinal or femoral herniation may occur. Reasons to suspect these injuries include blood in the urine; severe abdominal pain and tenderness (in the event of a bladder injury); persistent nausea, vomiting, or abdominal distention; and swelling in the femoral triangle or inguinal area (in the event of a hernia). All of these symptoms merit immediate medical evaluation in a hospital setting.

PreviousNextDiagnostic Tests

Plain radiography, technetium-99 (99 Tc) methylene diphosphonate (MDP) bone scanning, ultrasonography, nerve conduction studies, peritoneal radiography, computed tomography (CT) scanning, and MRI may be useful in the diagnosis of groin injuries.

Plain radiographs may show established osteitis pubis, a stress fracture (later stages), osteomyelitis (later stages), a slipped femoral epiphysis (epiphysiolysis), or osteoarthritis. Plain radiographs are useful in demonstrating the presence of hip abnormalities; one study found that 72% of male and 50% of female athletes evaluated with plain radiography demonstrated some evidence of radiographic hip abnormality, such as cam and pincer lesions associated with femoroacetabular impingement.[31]

A99m Tc-MDP bone scan may show osteitis pubis, a stress fracture, osteomyelitis, synovitis (occasionally bursitis), sacroiliitis, a tenoperiosteal lesion, or a muscle tear.

Ultrasonograms may show a muscle tear, hematoma, inguinal hernia, or bursitis (occasionally). Dynamic evaluation of the anatomic structures in the groin area through ultrasonography adds a significant amount of information to the imaging diagnosis, most notably in the evaluation of groin hernias.[32]

Nerve conduction studies may show ilioinguinal neuropathy or obturator neuropathy.

Peritoneal radiographs may show any inguinal hernia.

CT scans and MRIs may show AVN of the femoral head, disc pathology, radicular lesions, osteitis pubis, and other bone and soft-tissue injuries, as mentioned above. MRI with gadolinium has proven to be extremely valuable in the diagnosis of radiographically occult osseous abnormalities as well as soft tissue injuries like pubalgia, musculotendinous abnormalities, and bursitis.[33] MRI has been found to be 98% sensitive and 89-100% specific for injuries that involve the rectus abdominis, adductor tendon origins, and articular disease of the pubic symphysis.[33] Magnetic resonance arthrography (MRA) in the evaluation of intra-articular hip pain has been shown to be the best imaging modality for assessment of labral pathology (acetabular labral tears).[33]

Previous, Groin Injury

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Contusions

Background

Muscle contusion indicates a direct, blunt, compressive force to a muscle. Contusions are one of the most common sports-related injuries.[1, 2, 3] The severity of contusions ranges from simple skin contusions to muscle and bone contusions to internal organ contusions.

Although all tissue and organ contusions can result from traumatic sports injury, this article focuses on muscle contusions. Contusions of internal organs and bone contusions are not discussed in this article (see the Medscape Reference articles Concussion, Sacroiliac Joint Injury, Femur Injuries and Fractures, and Hip Pointer).

For excellent patient education resources, visit eMedicineHealth's Skin Conditions and Beauty Center and Eye and Vision Center. Also, see eMedicineHealth's patient education articles Bruises and Black Eye.

NextEpidemiologyFrequencyUnited States

Contusions and strain injuries comprise approximately 60-70% of all sports-related injuries. In addition, most contusion injuries go unreported and untreated. Documented muscle contusions account for one third of all sports injuries. The quadriceps and gastrocnemius muscle groups are most often involved (see the images below).[4, 5, 6, 7]

Athlete with a quadriceps strain. Place knee passively in 120º of flexion and immobilize with a double elastic wrap in a figure-8 fashion. This should occur within minutes of the injury. Used with permission courtesy of John Aronen, MD. Modified treatment of quadriceps contusion. Used with permission courtesy of John Aronen, MD.

Rotator cuff contusions of the shoulder have also been seen in professional football players. Cohen et al evaluated the incidence, treatment, and magnetic resonance imaging (MRI) appearance of players sustaining such injuries in a North American professional football team.[8] . The team's injury records from 1999 to 2005 were retrospectively reviewed for athletes who had sustained a rotator cuff contusion of the shoulder during in-season participation.

The investigators reported 26 players had a rotator cuff contusion, with an average of 5.5 rotator cuff contusions per season (47% of all shoulder injuries), 70.3% of which the predominant mechanism of injury was a direct blow. MRI findings included peritendon edema at the myotendinous junction, critical zone tendon edema, and subentheseal bone bruises.[8]

All patients were treated with a protocol involving modalities and cuff rehabilitation; 6 patients had persistent pain and weakness for at least 3 days and were given a subacromial corticosteroid injection. Overall, 3 patients (11.4%) required later surgical treatment on the shoulder.[8]

Cohen et al determined that rotator cuff contusions composed nearly half of all shoulder injuries in the football players in their study,[8] but the majority of affected athletes are able to return to sports with conservative treatment. A minority of shoulders might progress to more severe injuries such as rotator cuff tears. See the images below.

Rotator cuff injury. In this patient's shoulder radiography, the humeral head no longer matches up with the glenoid because the rotator cuff is torn and the strong deltoid muscle is pulling the head superiorly toward the acromion. Courtesy of Dr Thomas Murray, Orthopaedic Associates of Portland. International

The international frequency of contusions is similar to that in the United States.

PreviousNextFunctional Anatomy

Skeletal muscle constitutes the largest tissue mass in the body, comprising up to 45% of the total body weight. Muscles that cross a single joint are located close to bone, are frequently responsible for postural maintenance, and are most susceptible to contusions. On the other hand, 2-joint muscles, such as the rectus femoris muscle, lie more superficial and are more susceptible to stretch-induced strain injury.

Contusions are caused by blunt trauma to the outer aspect of the muscle, resulting in tissue and cellular damage and bleeding deep within the muscle and between the muscle planes.[1] The resultant tissue necrosis and hematoma lead to inflammation.[9] Little is known about the role of the inflammatory process and its importance in the healing process. Clearly, too much inflammation is unfavorable, but too little may be just as devastating.

A bruise is caused by blood that has escaped from damaged capillaries into the interstitial tissues. Within a few hours after the injury, the presence of necrotic tissue and hematoma initiates an inflammatory reaction. Because inflammation initiates macrophage action with subsequent phagocytosis of necrotic debris and stimulation of capillary production, it is vital to the process of muscle regeneration. However, inflammation invariably causes edema that leads to anoxia and further cell death.

The extent of the inflammatory response is often considered excessive and detrimental to muscle regeneration. However, controversy exists regarding this theory, because some literature indicates a worsened long-term outcome in patients placed on anti-inflammatory medications. Controversy also surrounds cryotherapy, with some literature touting its benefits, whereas others question its utility.[10, 11, 12]

PreviousProceed to Clinical Presentation , Contusions

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Exercise Physiology

Overview

Exercise represents one the highest levels of extreme stresses to which the body can be exposed. For example, in a person who has an extremely high fever approaching the level of lethality, the body metabolism increases to approximately 100% above normal; by comparison, the metabolism of the body during a marathon race increases to 2000% above normal.[1, 2, 3]

The following illustration depicts the cell structures of the skeletal muscle.

Excitation contraction coupling. DHP is dihydropyridine.

This article describes the basic physiology of exercise. The focus of this article is mainly at a subspecialty level; however, more detailed descriptions of various basic mechanisms are also provided for the casual reader.

For excellent patient education resources, visit eMedicineHealth's Healthy Living Center. Also, see eMedicineHealth's patient education articles Walking for Fitness and Resistance Training.

NextBasic Concepts -- Sex Differences

In general, the exercise-related measurements established for women follow the same general principles as those established for men, except for the quantitative differences caused by differences in body size, body composition, and levels of testosterone.

In women, the values of muscle strength, pulmonary ventilation, and cardiac output (all variables related with muscle mass) are generally 60-75% of the exercise physiology values recorded in men. When measured in terms of strength per square centimeter, the female muscle can achieve the same force of contraction as that of a male.[4, 5]

PreviousNextMusculoskeletal SystemFunctions of Muscle Tissue

Muscle tissue has 4 characteristics[1, 2, 3] that assume roles in homeostasis, as follows:

Excitability – Property of receiving and responding to stimuli such as the following: Neurotransmitters: Acetylcholine (ACh) stimulates skeletal muscle to contract.Electrical stimuli: Applying electrical stimuli between cardiac and smooth muscle cells causes the muscles to contract. Applying a shock to skeletal muscle causes contraction. Hormonal stimuli: Oxytocin stimulates smooth muscle in the uterus to contract during labor.Contractility – Ability to shortenExtensibility – Ability to stretch without damageElasticity – Ability to return to original shape after extension

Through contraction, muscle provides motion of the body (skeletal muscle), motion of blood (cardiac muscle), and motion of hollow organs such as the uterus, esophagus, stomach, intestines, and bladder (smooth muscle).

Muscle tissue also helps maintain posture and produce heat. A large amount of body heat is produced by metabolism and by muscle contraction. Muscle contraction during shivering warms the body.

Histology of Skeletal Muscle Tissue

Skeletal muscle consists of fibers (cells).[1, 2, 3] These cells are up to 100 µm in diameter and often are as long as the muscle. Each contains sarcoplasm (cytoplasm) and multiple peripheral nuclei per fiber. Skeletal muscle is actually formed by the fusion of hundreds of embryonic cells. Other cell structures (see image below) include the following:

Excitation contraction coupling. DHP is dihydropyridine. Each fiber is covered by a sarcolemma (plasma membrane).The sarcoplasmic reticulum (smooth endoplasmic reticulum) stores calcium, which is released into the sarcoplasm during muscle contraction. Transverse tubules (T tubules), which are extensions of the sarcolemma that penetrate cells, transmit electrical impulses from the sarcolemma inward, so electrical impulses penetrate deeply into the cell. Besides conducting electricity along their walls, T tubules contain extracellular fluid rich in glucose and oxygen. The sarcoplasm of fiber is rich in glycogen (glucose polymer) granules and myoglobin (oxygen-storing protein). It also is rich in mitochondria.

Each fiber contains hundreds to thousands of rodlike myofibrils, which are bundles of thin and thick protein chains termed myofilaments. From a cross-sectional view of a myofibril, each thick filament is surrounded by a hexagonal array of 6 thin filaments. Each thin filament is surrounded by a triangular array of thick filaments.

Thin myofilaments are composed of 3 proteins: actin, tropomyosin, and troponin (see image below).Thin filament. Thick myofilaments consist of bundles of approximately 200 myosin molecules (see image below). Myosin molecules look like double-headed golf clubs (both heads at the same end). The heads of the golf clubs are called myosin heads; they are also called cross-bridges because they link thick and thin filaments during contraction. They contain actin and adenosine triphosphate (ATP) binding sites. Myosin heads project out from the thick filaments, allowing them to bind to the thin filaments during contraction. Thick filament. Actin is a long chain of multiple globular proteins, similar in shape to kidney beans. Each globular subunit contains a myosin-binding site. Tropomyosin is a long strand of protein that covers the myosin-binding sites on actin when the muscle is relaxed.Troponin is a polypeptide complex that binds to tropomyosin, helping to position it over the myosin-binding sites on actin. During muscle contraction, calcium binds troponin, which causes tropomyosin to roll off of the myosin binding sites on actin.

Muscle contraction (overview of the sliding filament mechanism)

A muscle action potential travels over sarcolemma and enters the T tubules, causing the sarcoplasmic reticulum to release calcium into the sarcoplasm. This triggers the contractile process.

Myosin cross-bridges pull on the actin myofilaments, causing the thin myofilaments of a sarcomere to slide toward the centers of the H zones, as shown below.

Sarcomere. Other Components of Skeletal Muscle

Connective-tissue components

Deep fascia is a broad band of dense irregular connective tissue beneath and around muscle and organs.[1, 2, 3] Deep fascia is different from superficial fascia, which is loose areolar connective tissue.

Other connective-tissue components (all are extensions of deep fascia) include epimysium, which covers the entire muscle; perimysium, which penetrates into muscle and surrounds bundles of fibers called fascicles; and endomysium, which is delicate, barely visible, loose areolar tissue covering individual fibers (ie, individual cells).

Tendons and aponeuroses are tough extensions of epimysium, perimysium, and endomysium. Tendons and aponeuroses are made of dense regular connective tissue and attach the muscle to bone or other muscle. Aponeuroses are broad, flat tendons. Tendon sheaths contain synovial fluid and enclose certain tendons. Tendon sheaths allow tendons to slide back and forth next to each other with lower friction. Tenosynovitis is inflammation of the tendon sheaths and tendons, especially those of the wrists, shoulders, and elbows. Tendons are not contractile and not very stretchy; furthermore, they are not very vascular and they heal poorly.

Nerve and blood supply

Nerves convey impulses for muscular contraction. Nerves are bundles of nerve cell processes. Each nerve cell process (ie, axon) divides at its tip into a few to 10,000 branches called telodendria. At the end of each of these branches is an axon terminal that is rich in neurotransmitters.

Blood provides nutrients and oxygen for contraction. An artery and a vein usually accompany a nerve that penetrates skeletal muscle. Arteries in muscles dilate during active muscular activity, thus increasing the supply of oxygen and glucose.

Motor units

A motor nerve is a bundle of axons that conducts nerve impulses away from the brain or spinal cord toward muscles. Each axon transmits an action potential (ie, nerve impulse), which is a burst of electricity. The nerve impulse travels along the axons at a steady rate, like fire travels along a fuse; however, nerve impulses travel extremely fast. Each axon has 4-2000 or more branches (ie, telodendria), with an average of 150 telodendria. Each separate branch supplies a separate muscle cell. Thus, if an axon has 10 branches, it supplies 10 muscle fibers. Small motor units are for fine control of muscles; large motor units are for muscles that do not require such fine control.

Neuromuscular junction

The neuromuscular junction is made of an axon terminal and the portion of the muscle fiber sarcolemma it nearly touches (called the motor endplate). The neurotransmitter released at the neuromuscular junction in skeletal muscle is ACh. The motor endplate is rich in thousands of ACh receptors; the receptors are integral proteins containing binding sites for ACh and sodium channels.

Physiology of ContractionNerve impulse (action potential) reaches the axon terminal, which triggers calcium influx into the axon terminal.[1, 2, 3] Calcium influx causes synaptic vesicles to release ACh via exocytosis.ACh diffuses across synaptic cleft.ACh binds to the ACh receptor on the sarcolemma. Succinylcholine, a drug used to induce paralysis during surgery, binds to ACh receptors more tightly than ACh. Succinylcholine initially causes some depolarization, but then it binds to the receptor, preventing ACh from binding. Therefore, it blocks the muscle's stimulation by ACh, causing paralysis. Another drug that acts in a similar fashion is curare. These drugs do not cause pain relief or unconsciousness; thus, they are combined with other drugs during surgery. When ACh binds the receptor, it opens chemically regulated ion channels, which are sodium channels through the receptor molecule. Sodium, which is in high concentration outside cells and in low concentration inside cells, rushes into the cell through the channels. The cell, whose resting membrane potential along the inside of the membrane is negative when compared with the outside of the membrane, becomes positively charged along the inside of the membrane when sodium (a positive ion) rushes in. This change from a negative charge to a positive charge along the inner membrane is termed depolarization. The depolarization of one region of the sarcolemma (the motor endplate) initiates an action potential, which is a propagating wave of depolarization that travels (propagates) along the sarcolemma. Regions of membrane that become depolarized rapidly restore their proper ionic concentrations along their inner and outer surfaces in a process termed repolarization. (This process of depolarization, propagation, and repolarization is similar to dominoes that topple each other but also spring back into the upright position shortly afterward.) The action potential also propagates along the membrane lining the T tubules entering the cell.This action potential traveling along the T tubules causes the sarcoplasmic reticulum to release calcium into sarcoplasm.Calcium binds with troponin, causing it to pull on tropomyosin to change its orientation, exposing myosin-binding sites on actin. An ATPase, which also functions as a myosin cross-bridging protein, splits ATP into adenosine diphosphate (ADP) + phosphate (P) in the previous contraction cycle. This energizes the myosin head. The energized myosin head, or cross-bridge, combines with myosin-binding sites on actin. Power stroke occurs. The attachment of the energized cross-bridge triggers a pivoting motion (ie, power stroke) of the myosin head. During the power stroke, ADP and P are released from the myosin cross-bridge. The power stroke causes thin actin myofilaments to slide past thick myosin myofilaments toward the center of the A bands (see the following image). Sarcomere. ATP attaches to the myosin head again, allowing it to detach from actin. (In rigor mortis, an ATP deficiency occurs. Cross-bridges remain, and the muscles are rigid.) ATP is broken down to ADP and P, which cocks the myosin head again, preparing it to perform another power stroke if needed.Repeated detachment and reattachment of the cross-bridges results in shortening without much increase in tension during the shortening phase (isotonic contraction) or results in increased tension without shortening (isometric contraction). Release of the enzyme acetylcholinesterase in the neuromuscular junction destroys ACh and stops the generation of a muscle action potential. Calcium is taken back up (resequestered) in the sarcoplasmic reticulum, and myosin cross-bridges separate. ATP is required to separate myosin-actin cross-bridges. The muscle fiber resumes its resting state. Muscle Metabolic Systems During Exercise

The chemical energy that fuels muscular activities is ATP.[1, 2, 3] For the first 5 or 6 seconds of muscle power, muscular activity can depend on the ATP that is already present in the muscle cells. Beyond this time, new amounts of ATP must be formed to enable the activation of muscular contractions that are needed to support longer and more vigorous physical activities.

For activities that require a quick burst of energy that cannot be supplied by the ATP present in the muscle cells, the next 10-15 seconds of muscle power can be provided through the body’s use of the phosphagen system, which uses a substance called creatine phosphate to recycle ADP into ATP.[6] For longer and more intense periods of physical activity, the body must rely on systems that break down the sugars (glucose) to produce ATP.

The complete breakdown of glucose occurs in 2 ways: through anaerobic respiration (does not use oxygen) and through aerobic respiration (occurs in the presence of oxygen). The anaerobic use of glucose to form ATP occurs as the body increases its muscle use beyond the capability of the phosphagen system to supply energy. In particular, the glycogen lactic acid system, through its anaerobic breakdown of glucose, provides approximately 30-40 seconds more of maximal muscle activity. For this system, each glucose molecule is split into 2 pyruvic acid molecules, and energy is released to form several ATP molecules, providing the extra energy. Then, the pyruvic acid partially breaks down further to produce lactic acid. If the lactic acid is allowed to accumulate in the muscle, one experiences muscle fatigue. At this point, the aerobic system must activate.

The aerobic system in the body is used for sports that require an extensive and enduring expenditure of energy, such as a marathon race. Endurance sports absolutely require aerobic energy. A large amount of ATP must be provided to muscles to sustain the muscle power needed to perform such events without an excessive production of lactic acid. This can only be accomplished when oxygen in the body is used to break down the pyruvic acid (that was produced anaerobically) into carbon dioxide, water, and energy by way of a very complex series of reactions known as the citric acid cycle. This cycle supports muscle usage for as long as the nutrients in the body last.

The breakdown of pyruvic acid requires oxygen and slows or eliminates the accumulation of lactic acid. In summary, the 3 different muscle metabolic systems that supply the energy required for various activities are as follows:

Phosphagen system (for 10- to 15-sec bursts of energy)Glycogen lactic acid system (for another 30-40 sec of energy)Aerobic system (provides a great deal of energy that is only limited by the body's ability to supply oxygen and other important nutrients)

Many sports require the use of a combination of these metabolic systems. By considering the vigor of a sports activity and its duration, one can estimate very closely which of the energy systems are used for each activity.

Postexercise Recovery

Oxygen debt

During muscular exercise, blood vessels in muscles dilate and blood flow is increased in order to increase the available oxygen supply.[1, 2, 3] Up to a point, the available oxygen is sufficient to meet the energy needs of the body. However, when muscular exertion is very great, oxygen cannot be supplied to muscle fibers fast enough, and the aerobic breakdown of pyruvic acid cannot produce all the ATP required for further muscle contraction.

During such periods, additional ATP is generated by anaerobic glycolysis. In the process, most of the pyruvic acid produced is converted to lactic acid. Although approximately 80% of the lactic acid diffuses from the skeletal muscles and is transported to the liver for conversion back to glucose or glycogen, some lactic acid accumulates in muscle tissue, making muscle contraction painful and causing fatigue. Ultimately, once adequate oxygen is available, lactic acid must be catabolized completely into carbon dioxide and water.

After exercise has stopped, extra oxygen is required to metabolize lactic acid; to replenish ATP, phosphocreatine, and glycogen; and to replace (“pay back”) any oxygen that has been borrowed from hemoglobin, myoglobin (an iron-containing substance similar to hemoglobin that is found in muscle fibers), air in the lungs, and body fluids. The additional oxygen that must be taken into the body after vigorous exercise to restore all systems to their normal states is called oxygen debt. The debt is paid back by labored breathing that continues after exercise has stopped. Thus, the accumulation of lactic acid causes hard breathing and sufficient discomfort to stop muscle activity until homeostasis is restored.[7]

Recovery of muscle glycogen postexercise

Eventually, muscle glycogen must also be restored. Restoration of muscle glycogen is accomplished through diet and may take several days, depending on the intensity of exercise. The maximum rate of oxygen consumption during the aerobic catabolism of pyruvic acid is called maximal oxygen uptake.

Maximal oxygen uptake is determined by sex (higher in males), age (highest at approximately age 20 y), and size (increases with body size). Highly trained athletes can have maximal oxygen uptakes that are twice that of average people, probably owing to a combination of genetics and training. As a result, highly trained athletes are capable of greater muscular activity without increasing their lactic acid production and have lower oxygen debts, which is why they do not become short of breath as readily as untrained individuals.

Fuel Usage

Fuel usage (light exercise)

The best examples of light exercise are walking and light jogging.[1, 2, 3] The muscles that are recruited during this type of exercise are those that contain a large amount of type I muscle cells, and, because these cells have a good blood supply, it is easy for fuels and oxygen to travel to the muscle. ATP consumption makes ADP available for new ATP synthesis.

The presence of ADP (and the resulting synthesis of ATP) simulates the movement of hydrogen (H+) into the mitochondria; this, in turn, reduces the proton gradient and thus stimulates electron transport. The hydrogen on the reduced form of nicotinamide adenine dinucleotide (NADH) is used up, nicotinamide adenine dinucleotide (NAD) becomes available, and fatty acids and glucose are oxidized.

Incidentally, the calcium released during contraction stimulates the enzymes in the Krebs cycle and stimulates the movement of the glucose transporter 4 (GLUT-4) from inside of the muscle cell to the cell membrane. Both these exercise-induced responses augment the elevation in fuel oxidation caused by the increase in ATP consumption.

Fuel usage (moderate exercise)

An increase in the pace of running simply results in an increased rate of fuel consumption, an increased fatty acid release, and, therefore, an increase in the rate of muscle fatty acid oxidation. However, if the intensity of the exercise increases even further, a stage is reached in which the rate of fatty acid oxidation becomes limited.

The reasons why the rate of fatty acid oxidation reaches a maximum are not clear, but it is possible that the enzymes in the beta-oxidation pathway are saturated (ie, they reach a stage in which their maximal velocity [Vmax] is less than the rate of acetyl-coenzyme A [acetyl-CoA] consumption in the Krebs cycle). Alternatively, it may be that the availability of carnitine (the chemical required to transport the fatty acids into the mitochondria) becomes limited.

Whatever the reason, the consequence is that as the pace rises, the demand for acetyl-CoA cannot be met by fatty acid oxidation alone. The accumulation of acetyl-CoA that was so effective at inhibiting the oxidation of glucose is no longer present, so pyruvate dehydrogenase starts working again and pyruvate is converted into acetyl-CoA. In other words, more of the glucose that enters the muscle cell is oxidized fully to carbon dioxide. Therefore, the energy used during moderate exercise is derived from a mixture of fatty acid and glucose oxidation.

Fuel usage (strenuous exercise)

As the intensity of the exercise increases even further (ie, running at the pace of middle-distance races), the rate at which the muscles can extract glucose from the blood becomes limited. In other words, the rate of glucose transport reaches Vmax, either because the blood cannot supply the glucose fast enough or the number of GLUT-4s becomes limited. ATP generation cannot be serviced completely by exogenous fuels, and ATP levels decrease. Not only does this stimulate phosphofructokinase, it also stimulates glycogen phosphorylase. This means that glycogen stored within the muscle cells is broken down to provide glucose. Therefore, the fuel mix during strenuous exercise is composed of contributions from blood-borne glucose and fatty acids and from endogenously stored glycogen.

Fuel usage in individuals who are unfit

Being fit (biochemically speaking) means that the individual has a well-developed cardiovascular system that can efficiently supply nutrients and oxygen to the muscles. Fit people have muscle cells that are well perfused with capillaries (ie, they have a good muscle blood supply). Their muscle cells also have a large number of mitochondria, and those mitochondria have a high activity of Krebs cycle enzymes, electron transport carriers, and oxidation enzymes.

Individuals who are unfit must endure the consequences of a poorer blood supply, fewer mitochondria, less electron transport units, a lower activity of the Krebs cycle, and poorer activity of beta-oxidation enzymes. To generate ATP in the mitochondria, a steady supply of fuel and oxygen and decent activity of the oxidizing enzymes and carriers are needed. If any of these components are lacking, the rate at which ATP can be produced by mitochondria is compromised. Under these circumstances, the production of ATP by aerobic means is not sufficient to provide the muscles with sufficient ATP to sustain contractions. The result is anaerobic ATP generation using glycolysis. Increasing the flux through glycolysis but not increasing the oxidative consumption of the resulting pyruvate increases the production of lactate.

PreviousNextPulmonary Physiology During Exercise

The purpose of respiration is to provide oxygen to the tissues and to remove carbon dioxide from the tissues.[1, 2, 3] To accomplish this, 4 major events must be regulated, as follows:

Pulmonary ventilationDiffusion of oxygen and carbon dioxide between the alveoli and the bloodTransport of oxygen and carbon dioxide in the blood and body fluids and to and from the cellsRegulation of ventilation and other aspects of respiration: Exercise causes these factors to change, but the body is designed to maintain homeostasis.

When one goes from a state of rest to a state of maximal intensity of exercise, oxygen consumption, carbon dioxide formation, and total pulmonary and alveolar ventilation increase by approximately 20-fold. A linear relationship exists between oxygen consumption and ventilation. At maximal exercise, pulmonary ventilation is 100-110 L/min, whereas maximal breathing capacity is 150-170 L/min. Thus, the maximal breathing capacity is approximately 50% greater than the actual pulmonary ventilation during maximal exercise. This extra ventilation provides an element of safety that can be called on if the situation demands it (eg, at high altitudes, under hot conditions, abnormality in the respiratory system). Therefore, the respiratory system itself is not usually the most limiting factor in the delivery of oxygen to the muscles during maximal muscle aerobic metabolism.

VO2max is the rate of oxygen consumption under maximal aerobic metabolism. This rate in short-term studies is found to increase only 10% with the effect of training. However, that of a person who runs in marathons is 45% greater than that of an untrained person. This is believed to be partly genetically determined (eg, stronger respiratory muscles, larger chest size in relation to body size) and partly due to long-term training.

Oxygen diffusing capacity is a measure of the rate at which oxygen can diffuse from the alveoli into the blood. An increase in diffusing capacity is observed in a state of maximal exercise. This results from the fact that blood flow through many of the pulmonary capillaries is sluggish in the resting state. In exercise, increased blood flow through the lungs causes all of the pulmonary capillaries to be perfused at their maximal level, providing a greater surface area through which oxygen can diffuse into the pulmonary capillary blood. Athletes who require greater amounts of oxygen per minute have been found to have higher diffusing capacities, but the exact reason why is not yet known. Although one would expect the oxygen pressure of arterial blood to decrease during strenuous exercise and carbon dioxide pressure of venous blood to increase far above normal, this is not the case. Both of these values remain close to normal.

Stimulatory impulses from higher centers of the brain and from joint and muscle proprioceptive stimulatory reflexes account for the nervous stimulation of the respiratory and vasomotor center that provides almost exactly the proper increase in pulmonary ventilation to keep the blood respiratory gases almost normal. If nervous signals are too strong or weak, chemical factors bring about the final adjustment in respiration that is required to maintain homeostasis.

PreviousNextCardiovascular System and Exercise

Regular exercise makes the cardiovascular system more efficient at pumping blood and delivering oxygen to the exercise muscles.[1, 2, 3, 8, 9, 10] Releases of adrenaline and lactic acid into the blood result in an increase of the heart rate (HR).

Basic definitions of terms are as follows:

VO2 equals cardiac output times oxygen uptake necessary to supply oxygen to muscles.The Fick equation is the basis for determination of VO2 (see image below).[10] Fick equation.

Exercises increase some of the different components of the cardiovascular system, such as stroke volume (SV), cardiac output, systolic blood pressure (BP), and mean arterial pressure. A greater percentage of the cardiac output goes to the exercising muscles. At rest, muscles receive approximately 20% of the total blood flow, but during exercise, the blood flow to muscles increases to 80-85%.

To meet the metabolic demands of skeletal muscle during exercise, 2 major adjustments to blood flow must occur. First, cardiac output from the heart must increase. Second, blood flow from inactive organs and tissues must be redistributed to active skeletal muscle.

Generally, the longer the duration of exercise, the greater the role the cardiovascular system plays in metabolism and performance during the exercise bout. An example would be the 100-meter sprint (little or no cardiovascular involvement) versus a marathon (maximal cardiovascular involvement).

General functions of the cardiovascular system

The cardiovascular system helps transport oxygen and nutrients to tissues, transport carbon dioxide and other metabolites to the lungs and kidneys, and distribute hormones throughout the body. The cardiovascular system also assists with thermoregulation.

Cardiac cycle

The pumping of blood by the heart requires the following 2 mechanisms to be efficient:

Alternate periods of relaxation and contraction of the atria and ventriclesCoordinated opening and closing of the heart valves for unidirectional flow of blood

The cardiac cycle is divided into 2 phases: ventricular diastole and ventricular systole.

Ventricular diastole This phase begins with the opening of the atrioventricular (AV) valves. The mitral valve (located between the left atrium and left ventricle) opens when the left ventricular pressure falls below the left atrial pressure, and the blood from left atrium enters the left ventricle. Later, as the blood continues to flow into the left ventricle, the pressure in both chambers tends to equalize.At the end of the diastole, left atrial contractions cause an increase in left atrial pressure, thus again creating a pressure gradient between the left atrium and ventricle and forcing blood into the left ventricle. Ventricular systole Ventricular systole begins with the contraction of the left ventricle, which is caused by the spread of an action potential over the left ventricle. The contraction of the left ventricle causes an increase in the left ventricular pressure. When this pressure is higher than the left atrial pressure, the mitral valve is closed abruptly. The left ventricular pressure continues to rise after the mitral valve is closed. When the left ventricular pressure rises above the pressure in the aorta, the aortic valve opens. This period between the closure of the mitral valve and the opening of the aortic valve is called isovolumetric contraction phase. The blood ejects out of the left ventricle and into the aorta once the aortic valve is opened. As the left ventricular contraction is continued, 2 processes lead to a fall in the left ventricular pressure. These include a decrease in the strength of the ventricular contraction and a decrease in the volume of blood in the ventricle. When the left ventricular pressure falls below the aortic pressure, the aortic valve is closed. After the closure of the aortic valve, the left ventricular pressure falls rapidly as the left ventricle relaxes. When this pressure falls below the left atrial pressure, the mitral valve opens and allows blood to enter left ventricle. The period between the closure of the aortic valve closure and the opening of the mitral valve is called isovolumetric relaxation time. Right-sided heart chambers undergo the same phases simultaneously.Pressure changes during the cardiac cycle

Most of the work of the heart is completed when ventricular pressure exists. The greater the ventricular pressure, the greater the workload of the heart. Increases in BP dramatically increase the workload of the heart, and this is why hypertension is so harmful to the heart.

Arterial BP is the pressure that is exerted against the walls of the vascular system. BP is determined by cardiac output and peripheral resistance. Arterial pressure can be estimated using a sphygmomanometer and a stethoscope. The reference range for males is 120/80 mm Hg; the reference range for females is 110/70 mm Hg.

The difference between systolic and diastolic pressure is called the pulse pressure. The average pressure during a cardiac cycle is called the mean arterial pressure (MAP). MAP determines the rate of blood flow through the systemic circulation.

During rest, MAP = diastolic BP + (0.33 X pulse pressure). For example, MAP = 80 + (0.33 X [120-80]), MAP = 93 mm Hg.During exercise, MAP = diastolic BP + (0.50 X pulse pressure). For example, MAP = 80 + (0.50 X [160-80]), MAP = 120 mm Hg.Coordinated control of the heart

The heart has the ability to generate its own electrical activity, which is known as intrinsic rhythm. In the healthy heart, contraction is initiated in the sinoatrial (SA) node, which is often called the heart's pacemaker. If the SA node cannot set the rate, then other tissues in the heart are able to generate an electrical potential and establish the HR.

Control of cardiac output (HR)

The parasympathetic nervous system and the sympathetic nervous system affect a person's HR.

Parasympathetic nervous system: The vagus nerve originates in the medulla and innervates the SA and AV nodes. The nerve releases ACh as the neurotransmitter. The response is a decrease in SA node and AV node activity, which causes a decrease in HR. Sympathetic nervous system: The nerves arise from the spinal cord and innervate the SA node and ventricular muscle mass. The nerves release norepinephrine as the neurotransmitter. The response is an increase in HR and a force of contraction of the ventricles. Control of sympathetic and parasympathetic activity

At rest, sympathetic and parasympathetic nervous stimulation are in balance. During exercise, parasympathetic stimulation decreases and sympathetic stimulation increases. Several factors can alter sympathetic nervous system input.

Baroreceptors are groups of neurons located in the carotid arteries, the arch of aorta, and the right atrium. These neurons sense changes in pressure in the vascular system. An increase in BP results in an increase in parasympathetic activity except during exercise, when the sympathetic activity overrides the parasympathetic activity.

Chemoreceptors are groups of neurons located in the arch of the aorta and the carotid arteries. These neurons sense changes in oxygen concentration. When oxygen concentration in the blood is decreased, parasympathetic activity decreases and sympathetic activity increases.

Temperature receptors are neurons located throughout the body. These neurons are sensitive to changes in body temperature. As temperature increases, sympathetic activity increases to cool the body and to reduce internal core temperature.

Control of cardiac output (SV)

SV is controlled by end-diastolic volume, average aortic BP, and the strength of ventricular contraction.

End-diastolic volume: This is often referred to as the preload. If the end-diastolic volume increases, the SV increases. With an increased end-diastolic volume, a slight stretching of the cardiac muscle fibers occurs, which increases the force of contraction Average aortic BP: This is often referred to as the afterload. The BP in the aorta represents a barrier to the blood being ejected from the heart. The SV is inversely proportional to the aortic BP. During exercise, the afterload is reduced, which allows for an increase in SV. Strength of ventricular contraction: Epinephrine and norepinephrine can increase the contractility of the heart by increasing the calcium concentration within the cardiac muscle fiber. Epinephrine and norepinephrine allow for greater calcium entry through the calcium channels in cardiac muscle fiber membranes. This allows for greater myosin and actin interaction and an increase in force production. Control of cardiac output (venous return)

Venoconstriction occurs as a response to sympathetic nervous system stimulation. Sympathetic stimulation constricts the veins that drain skeletal muscle. This causes greater blood to flow back to the heart.

The muscle pump is the rhythmic contraction and relaxation of skeletal muscle that compresses the veins and thus drains the skeletal muscle. This causes greater blood flow back to the heart. The muscle pump is very important during both resting and exercise conditions.

During exercise, the respiratory pump helps increase venous return. The pressure within the chest decreases and abdominal pressure increases with inhalation, thus facilitating blood flow back to the heart. Because of the increased respiratory rate and depth of breathing during exercise, this is an effective way to increase venous return.

Hemodynamics

The circulatory system is a closed-loop system, and flow through the circulatory system is the result of pressure differences between the 2 ends of the system, the left ventricle (90 mm Hg) and the right atrium (approximately 0 mm Hg).

Systemic blood flow affects hemodynamics. The control of blood flow during exercise is extremely important to ensure that blood and oxygen are transported to the tissues that need them most. Blood flow to tissues is dependent on the relationship between BP and the resistance provided by the blood vessels.

Blood flow at rest is equal to the change in pressure divided by the resistance of the vessels (ie, BF = P/R, where BF is blood flow, P is pressure, and R is resistance). Blood flow during exercise is regulated by changing BP and altering the peripheral resistance of the vessels.

The pressure change at rest in the cardiovascular system is 93 mm Hg, as follows: Mean aortic pressure = 93 mm Hg, mean right atrial pressure = 0 mm Hg, and driving pressure in the system = 93 mm Hg.

During exercise, BP increases so that blood flow through the body increases. Blood flow is also increased during exercise by decreasing the resistance of the vessels in the systemic circulation of active skeletal muscle. Resistance is determined by the following formula:

Resistance = (length of tube X viscosity of blood)/radius4.

Changing the radius of the vessels has the most profound effect on blood flow. Doubling the radius of a blood vessel decreases resistance by a factor of 16. Decreasing the radius of a blood vessel by half increases resistance by a factor of 16. The arterioles have the most control over blood flow in the systemic circulation.

Changes in oxygen delivery to muscle during exerciseBP increases as exercise intensity increases, rising from approximately 120 mm Hg to approximately 200 mm Hg.SV increases during exercise until 40% of VO2max (maximum oxygen uptake level) is reached, rising from approximately 80 mL/beat to approximately 120 mL/beat.HR increases with intensity until VO2max is reached, rising from approximately 70 beats per minute to approximately 200 beats per minute.Cardiac output increases with intensity until VO2max is reached, rising from approximately 5 L/min to approximately 25-30 L/min.

The arterial-venous oxygen difference is the amount of oxygen extracted from the blood as it passes through the capillary bed. This difference rises from approximately 4 mL of oxygen per 100 mL of blood at rest to approximately 18 mL of oxygen per 100 mL of blood during high-intensity aerobic exercise.

Redistribution of blood flow during exercise

At rest, 15-20% of blood goes to skeletal muscle; during exercise, this amount increases to 80-85%. The percentage of blood to the brain decreases, but the absolute amount increases. The same percentage of blood goes to cardiac muscle, but the absolute amount increases. Blood flow to visceral tissues and inactive skeletal muscle reduces. In addition, the cutaneous blood flow initially decreases, but it later increases during the course of exercise.

The redistribution of the blood is brought about by several mechanisms. During exercise, generalized vasodilatation occurs because of the accumulation of vasodilatory metabolites. This leads to a decrease in the peripheral resistance, which, in turn, elicits a strong increase in the sympathetic activity through the activation of baroreceptors. The increase in sympathetic activity leads to vasoconstriction in the visceral organs, whereas the vasodilatation predominates in the blood vessels of the muscles and the coronary circulation because of the local vasodilatory metabolites. The cutaneous blood vessels initially respond to the sympathetic activity by vasoconstriction. As the exercise continues, temperature reflexes are activated and cause cutaneous vasodilatation to dissipate the heat produced by the muscle activity, resulting in an increase in the cutaneous blood flow.

Regulation of blood flow at the local level

The local blood flow is controlled by chemical factors, metabolites, paracrines, physical factors such as heat or cold, stretch effects on endothelial membrane, active hyperemia, and reactive hyperemia. The paracrine regulation is mainly regulated by nitric oxide, histamine release, and prostacyclin. Nitric oxide diffuses to smooth muscle and causes vasodilation by reducing calcium entry into smooth muscle.

Regulation of cardiovascular function

HR and blood flow are controlled by various centers in the brain. These centers receive input from receptors located throughout the body. The centers work to initiate the appropriate response from tissues and organs in the body.

Aerobic exercise requires oxygen to be present for the generation of energy from fuels such as glucose or glycogen. Aerobic exercise results in no buildup of lactic acid as a result of metabolism. This process is more efficient than anaerobic metabolism. During normal rest and aerobic exercise, carbohydrates and fats are used as fuels. A high degree of aerobic fitness requires a well-adapted ability to take in, carry, and use oxygen. Laboratory measurements are most accurate, but they are expensive. An individual's fitness level may be estimated according to these measurements.

Anaerobic exercise produces lactic acid and is usually of short duration. Anaerobic exercise is high intensity and has a greater inherent risk of injury. Individuals who are unfit have a lower anaerobic threshold than athletes who are aerobically trained. The well-trained athlete may be able to approach 80% of the VO2max aerobically without lactate production.

The usual VO2 measurements are in L/min; however, if the size of the individual needs to be accounted for, the measurements may be in mL/kg/min. The values for the average person aged 20 years are 37-48 mL/kg/min. Male athletes who are highly trained may approach measurements in the high 70s to low 80s. Training enhances the ability of the body, in particular the muscle cells, to better handle oxygen. Muscle must be able to use oxygen efficiently to keep anaerobic metabolism at a given level of effort to a minimum.

Cardiac output is a major determinant of oxygen uptake. VO2max declines with age as the maximum HR declines. This is one of the major factors causing the approximately 7% decline with each decade of life after age 30 years. Muscle training and use of oxygen at the end organ, muscle, is the second factor that affects oxygen uptake. The arterial-venous oxygen difference comes about as a combination of arterial oxygen content, shunting of blood to muscles, and the muscle extraction of oxygen.

Training results in a more efficient heart and an increase in the maximum SV. An increase in VO2 results in an ease in the stress of a given workload. When maximum SV is increased, the heart can work more efficiently at a given pulse rate. This lessens the necessity of an increased pulse at a given workload. Resting pulse is lower, as is the pulse at any given workload.

One metabolic unit (MET) equals the VO2 at rest. The estimate of the value of one MET is 3.5 mL of oxygen per kg/min. Conversion of VO2 measurements may be obtained by dividing the value of the VO2 in mL of oxygen per kg/min by the value of one MET or 3.5. For example, a VO2 measurement of 35 mL of oxygen per kg/min is equivalent to an output of 10 METs.

Cardiovascular changes with isometric exercise

Cardiovascular changes during isometric exercise differ from those during dynamic exercise. Static exercise causes compression of the blood vessels in the contracting muscles, leading to a reduction in the blood flow in them. Therefore, total peripheral resistance, which normally falls during dynamic exercise, does not fall and may, in fact, increase, especially if several large groups of muscles are involved in the exercise. The activation of the sympathetic system with exercise thus leads to an increase in HR, cardiac output, and BP.

Because the total peripheral resistance does not decrease, the increase in HR and cardiac output is less and an increase in the systolic, diastolic, and mean arterial pressure is more compared with those seen with dynamic exercise. Because BP is a major determinant of afterload, the left ventricular wall stress, and thus the cardiac workload, is significantly higher during static exercise compared with the cardiac workload achieved during dynamic exercise.

Cardiac changes following training

In most cases, the SV plateaus at a VO2 of approximately 40-60% of the maximum. This applies to both trained and untrained males and females. The SV for untrained males may approach 100-120 mL/beat/min. For trained males, this value is 150-170 mL/beat/min. For highly trained athletes, maximal SV may reach or even exceed 200 mL/beat/min. The values for women are lower than those for men. Maximal SV for untrained women is usually between 80 mL/beat/min, and for trained women, it is usually between 100 mL/beat/min. These changes translate into an increase in the circulation blood volume and in cardiac output, with a corresponding decrease in the resting HR and the resting and exercise BP.

The heart undergoes certain morphologic changes in response to chronic exercise, commonly seen via echocardiography. These morphologic changes define what is commonly referred to as an "athletic heart." Athletic heart syndrome is characterized by hypertrophy of the myocardium (ie, an increase in the mass of the myocardium).

Although the hypertrophy in athlete's heart is morphologically similar to that seen in patients with hypertension, several important differences exist. In contrast to the hypertension-induced hypertrophy, the hypertrophy in the athletic heart is noted in absence of any diastolic dysfunction, with a normal isovolumetric relaxation time, with no decrease in the peak rate of left ventricular filling, and with no decrease in the peak rate of left ventricular cavity enlargement and wall thinning. Because the wall stress in the athlete's heart is normal, sometimes the hypertrophy seems to be disproportionate to the level of resting BP.

In addition, the rate of decline in the left ventricular hypertrophy and mass is much more rapid when the training is stopped compared with the regression in the same parameters in treated hypertension. On average, the decline in these parameters is seen 3 weeks after stopping exercise, and these morphologic changes can be seen on echocardiograms.

Sometimes, these morphologic changes are confused with the changes seen in patients with hypertrophic cardiomyopathy (HCM). A few important morphologic differences exist. In athletic heart syndrome, the hypertrophy is usually symmetrical, as opposed to the asymmetrical hypertrophy in HCM. Also, the left ventricular size is generally normal or increased, and the left atrial size is normal, as opposed to a small left ventricular cavity with a larger left atrial cavity size (usually >4.5 cm) in HCM. Despite these differences, sometimes making a distinction between 2 conditions is a challenge.

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In summary, exercise is accomplished by alteration in the body response to the physical stress (exercise physiology). These responses to exercise include an increase in the HR, BP, SV, cardiac output, ventilation, and VO2. The metabolism at the cellular level is also modulated to accommodate the demands of exercise. These changes occur temporarily during the exercise. Long-term changes also occur in the body metabolism and function.

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