There are injuries in medicine that are unique only to athletes, and there are unique injuries that are known only to sports medicine physicians. Bicycling injuries include both. Therefore the clinician caring for a cyclist must know both the sport and the bicycle.
With regard to the total number of sports injuries per year, cycling has the highest absolute number of injuries per year (614,594), followed by basketball (597,224) and football (372,380) (64). Bicycling also has been found to be the most common sports-related activity associated with injury among children aged 5 to 14 years, more than basketball, football, and playground equipment (14).
Cycling injuries can be classified into bicycle contact, traumatic, and overuse injuries. Most studies involve children and commuters. Only three epidemiological studies, all retrospective, have been conducted on professional cyclists (7,15,19). Definition of injury, severity, and specificity of diagnosis were different for all three. Studies on overuse injuries in recreational cyclists are often questionnaires of riders in multiday tours (18,39,67). Wilber et al. (68) reported on overuse injuries in a recreational club, and Baker (5) reported on traumatic injuries in a competitive Masters club. (Table 1)
Traumatic injuries occurred 48.5% and overuse injuries occurred 51.5% in one study of top level professionals (19). More than two-thirds of traumatic injuries occur in the upper extremity and two-thirds of overuse injuries occur in the lower extremity (19). In another study in elite professionals, 38% of injuries were traumatic and 62% of injuries were overuse (7). There are no known studies grouping bicycle contact injury separately from overuse injuries. Extrapolation of data from a study on nontraumatic injuries in amateur participants in a 500-mile 8-d tour revealed a 57.2% rate of bicycle contact injuries (32.8% buttock, 9.1% groin, 10% palmar, and 5.3% foot) versus 42.8% overuse (67). Injured elite cyclists seem better equipped to continue training than recreational riders (19). Stress fractures, commonly seen in runners, do not occur in cyclists. Muscle tears, common in runners from eccentric load, are rare in cyclists with high quadriceps concentric load.
Cyclists are exposed to high traumatic risk racing in a peloton, at high speeds, on various road and weather conditions. By stage 9 of the 2011 Tour de France, 14 fractures occurred and 16 riders retired from the race, with one athlete in an intensive care unit (29). In a 4-year study of 51 top level professionals, 43 cyclists experienced 103 injuries, with 50 (48.5%) traumatic injuries and 53 (51.5%) overuse injuries (19). Only eight cyclists (15.6%) were injury free. Twenty-two (43%) athletes experienced both overuse and traumatic injuries, while 13 (25.5%) experienced only traumatic lesions and 10 (19.5%) only overuse injuries. Twenty-nine cyclists (67.4%) experienced more than one injury. Twenty-eight fractures occurred, with the clavicle having the most common fracture (11 cases). The majority (68.5%) of overuse injuries was located in the lower limbs, most occurring during preseason. Severe injuries requiring more than 1 month off occurred in four cases, and all of them are trauma (8% of traumatic injuries) requiring surgery.
Bicycle Contact Injuries
Shoe Pedal Interface
Burning feet, “hot foot,” numbness, or pain is a common complaint as a result of compression of interdigital plantar nerves from a fixed cleat-pedal interface and narrow rigid cycling shoe. Diagnosis of Morton’s neuroma, a perineural fibroma commonly occurring between the third and fourth metatarsals, should be made only when seen on ultrasound or magnetic resonance imaging (MRI). On ultrasound, it appears as a noncompressible hypoechoic mass greater than 5 mm.
Symptoms may be relieved with cleat adjustment (usually with the cleat positioned further back), by wearing a shoe with a wider toe box, by loosening the straps on the shoes, or by using a wider pedal. A metatarsal pad and manual therapy may be tried. For recalcitrant cases, cortisone injection, prolotherapy, or sclerosing alcohol injections may be considered. Neurectomy, via plantar or dorsal approach, is the mainstay of surgical intervention.
A Cochrane database systemic review found limited studies and insufficient evidence with which to assess the effectiveness of surgical and nonsurgical interventions for Morton’s neuroma: “There is, at most, a very limited indication that transposition of the transected plantar digital nerve may yield better results than standard resection of the nerve in the long term. There are, at best, very limited indications to suggest that dorsal incisions for resection of the plantar digital nerve may result in less symptomatic postoperative scars when compared to plantar excision of the nerve” (65). Failure rates of primary neurectomy have been reported as high as 24% to 39% (40,69). Reported rates for restrictions in footwear are as high as 71% for patients after primary neurectomy (50). Revision neurectomy may fair even worse, with a 33% to 65% risk of chronic pain from scarring or amputation stump neuroma (37,43).
Moisture, friction, and pressure lead to skin ailments in the perineal region. Chafing is the most common ailment, relieved with brief time off and an emollient. Cycling in wet clothing, such as in triathlons or the rain, is a frequent cause of chafing. Ulceration from severe friction requires wound treatment. Saddle sores, ranging from furuncles and folliculitis to nodular induration, may limit riding for a prolonged period. They often require incision and drainage, or surgical excision for the more severe ischial hygroma or “third testicle” (accessory testicle or “biker’s nodule”) (28). Time off the bike, warm soaks, cortisone, or antifungal or antibacterial ointment may be considered. Prevention is paramount and involves riding in a dry, clean chamois and changing clothing immediately after cycling. Check saddle height and tilt, handlebar reach and height, and saddle type.
A significant percentage of body weight may be positioned on the bicycle saddle during seated bicycling depending on variables such as a rider’s position on the bike and rider effort. Regardless of the saddle design, it is the racing position of a cyclist, in an effort to get good aerodynamics by lowering the torso toward a horizontal flat back position and tilting the pelvis anteriorly, that transfers pressure from the ischial tuberosities to the perineum, where vascular and neural structures reside. Transcutaneous penile oxygen pressure (tPO2) monitoring, believed to correlate with penile blood flow, has been found to be a reliable method for measuring penile oxygen levels during cycling (12). A significant decrease in penile oxygen perfusion occurs during seated bicycling, with measurement as high as an 82% drop in tPO2 (60). The implications of decreased tPO2 over different time intervals when bicycling is unknown and needs to be further researched. Hypoxemia in the corpus cavernosum is associated with penile fibrosis, which is known to lead to erectile dysfunction (ED). ED rates have been reported to occur as high as 24% in amateurs with weekly mileage greater than 400 km (63).
Ischemic neuropathy may result also from compression of the neurovasculature in the perineum and in Alcock’s canal. Rates of genital numbness have been reported as low as 10% in amateurs on an 8-d ride of 500 miles to as high as 91% in a small study of 17 cycling policemen (67,59). “Cyclist’s syndrome” is a specific form of pudendal nerve entrapment related to prolonged bicycling resulting in pain, burning, and numbness, sometimes accompanied by sexual dysfunction, impotence, or urinary incontinence. The pathogenesis of pudendal neuropathy is unknown. Compression, friction, and stretching of nerves are implicated.
A rider’s position, bike fit, and riding technique play the greatest roles in prevention and treatment of perineal compression. Risk of compression is greatest during time trialing, in indoor riding on rollers or a trainer without frequent standing, in heavier cyclists, and in mountain biking. Preventive measures such as changing riding style, alternating standing, and sitting often are recommended. Riding on a recumbent bike causes no decrease in penile perfusion, as does standing while cycling. Three minutes of standing are required to produce stable increases in penile oxygen levels after seated compression (12). An excessively high saddle, narrow saddle, excessive saddle tilted up, or handlebars excessively forward or low can all increase compression. Ergonomic wider saddles, with a split saddle, chopped nose, or central cut out, have all been designed to decrease compression. Cohen and Gross (12) studied tPO2 in three racing saddle designs (a “standard” narrow saddle, a padded saddle with an elliptical hole in the center and a cutout seam in the nose, and a saddle with a split V in the rear and a central depression from the back to the tip of the nose) and found none of the saddles spared a drop in penile tPO2 (decreases of 76%, 73%, and 62%, respectively). Dettori (21) actually found an increased risk of ED with a cutout saddle among those who experienced numbness versus those who did not experience numbness, possibly due to compression on the cutout edge or decreased surface area. Time off the bike is warranted for prolonged compressive symptoms as irreversible neuropathy can occur (41). Physical therapy, manual therapy, and injection therapy are treatment options for relief of pain from neuralgia. The symptoms for most cyclists are transient, but the implications are unknown.
Hands Handlebar Interface
Ulnar neuropathy/carpal tunnel syndrome
Stiefler, in 1927, was the first to report on bicycling causing prolonged compression of the ulnar nerve (“cyclists palsy”), and it is less common in the median nerve (30,42). Twenty-three out of 25 cyclists on a 600-km ride experienced compressive neuropathy in their hands (45). Thirty-two of 89 (36%) cyclists on a tour of 80 d and 4500 miles experienced hand numbness, 10 (11%) in the median nerve distribution, with 1 unable to adduct his thumb, 1 unable to adduct his little finger, and 1 unable to abduct his little finger (39).
Mononeuropathy of the deep palmar branch of the ulnar nerve in Guyon’s canal may cause clawing. With a type I lesion, mixed sensory and motor, compression is proximal (outside of Guyon’s canal) and clawing usually is not seen (42). Isolated lesions of the deep terminal motor branch, with distal sensory branches intact, result in the athlete unaware of any compression until the motor lesion develops.
Increased compression occurs with prolonged riding without change in hand position, stationary biking, downhill cycling, rough terrain, handlebars too low or forward, poor padding in gloves or bars, or improper suspension or “death grip” (an overly tight grip on the handlebars caused by fear) in mountain biking. Most cases result in a transient neuropraxia, with full recovery with modification or cessation of activity. However rarely permanent damage may occur (30). Treatments for the cyclist include the following: reduction in training, changing hand position often, increasing padding in the bars or gloves, shortening the reach or raising the handlebars, or using clip-on aerobars.
Bicycle contact and overuse ailments may be addressed with bike fit adjustment as previously published by the author (61, Table 1). The order of fit is as follows: 1) foot-cleat-pedal interface, 2) pelvis-saddle interface, 3) hands-handlebar interface. The first metatarsal-phalangeal joint should lie directly over the pedal spindle. Saddle height is set so when the pedal is in the 6 o’clock or dead bottom center (BDC) position, the cyclist’s knee flexes 25° to 30°, corresponding to a saddle height of about 0.883× the rider’s inseam length in centimeter. When the pedal is in the 3 o’clock or knee over pedal spindle position, a plumb line dropped from the inferior pole of the patella should fall directly over the pedal spindle. Saddle tilt should be close to level. A rider’s torso should flex about 60° with the hands in the drops and about 45° when on the hoods. Stem height and length may require swapping out stems for a comfortable, powerful, and aerodynamic position. With correct frame size, stem height should be about 1 to 3 inches below saddle height and stem length about 10 to 12 cm.
Baker (5) reported on traumatic injuries on 85 cyclists in a racing Masters club. Seventy-nine percent were seen emergently for trauma, 33% were admitted to the hospital, and 15% were admitted to an intensive care unit. Fifty-four percent sustained fractures and 45% a head injury, 34% reported a concussion, and 9% sustained multiple concussions. Ninety percent experienced road rash. Sixty-nine percent of injuries occurred riding alone and 31% occurred riding in groups. Thirty-seven percent of solo road injuries were from crashes with motor vehicles, 9% from potholes, rocks, or dogs, 12% from operator errors (cornering too fast or adjusting parts while riding), and 10% by mechanical reasons (broken fork or flat tire). Of the injuries during group riding, 17% occurred riding in a pace line, most trying to avoid crashing into other crashed riders, with 12% in races, mostly criteriums.
Statistics on deaths from motor vehicle collisions specifically in athletes do not exist. Two deaths occur in bicyclists per day in the United States from motor vehicle collisions. Florida has three times the national rate (1). The typical striking vehicle is often a freight truck or large, expensive automobile, often occurring at dusk (1). Medium- and high-volume traffic areas carry a twofold increase in the odds of collision, with risk greatest at intersections, on divided roads, and near retail establishments (56). There is less risk bicycling on good road surfaces, with streetlights, and on multiuse paths versus sidewalks.
About 50% of traumatic cycling injuries result in fractures (19). The most common is the clavicle followed by the wrist, ribs, and elbow. Lower extremity fractures are rarer and often involve the pelvis, hip, or femur. Femur fractures are displaced usually, requiring surgery, while pelvis fractures are nondisplaced often, non-life threatening, and detected often with computed tomography (CT) or MRI after negative x-rays. Off-road cyclists in events appear to sustain more fractures, dislocations, and concussions than road cyclists in events (52).
Clavicle fractures/shoulder injuries
It is joked commonly, “If you race long enough, you will eventually break your collarbone.” Clavicle fractures are caused by a direct blow to the shoulder from falls, often going over the front end. They are associated often with concussions and rib fractures. Cyclists with clavicle fractures treated nonoperatively usually can ride a stationary trainer within 1 wk, ride outdoors within 2 to 3 wk, and race in 4 to 6 wk.
Most clavicle fractures are treated nonoperatively, except when communition, shortening, or severe displacement is present. Initial shortening of displaced middle third fractures greater than or equal to 20 mm was found to have a highly significant association with nonunion and unsatisfactory result (difficulty lifting heavy objects, pain, paresthesia, or cosmetic complaint) with closed treatment (32). Displacement of more than one bone width on initial x-ray (0° and 45° tilted view) in another study was found to be the strongest radiographic risk factor for persistent symptoms at 6 months with nonoperative treatment (49). Results of a meta-analysis of plating versus intramedullary pin and plating versus conservative treatment for midshaft fractures (4 studies involving 305 clavicle fractures selected for inclusion) found 1) no significant difference between plating and intramedullary pinning with regard to shoulder scores, nonunion, infection, fixation failure, and hardware removal; 2) more symptomatic hardware events with plating compared with intramedullary pinning; and 3) more cosmetic satisfaction and reduced nonunion, malunion, and neurologic symptoms with plating versus conservative treatment (22). Late repairs of painful nonunion or malunion displaced midshaft fractures also have been found to have similar results to immediate fixation (53). Fractures treated operatively may allow a cyclist to return to training sooner.
If there is suspicion of sternoclavicular (SC) joint injury, obtain a CT. Posterior dislocations should be reduced operatively. Delayed erosion into vessels and stroke has occurred in chronic SC posterior dislocations.
AC separations are equally common and all but the most severe grade 3 separations are treated nonoperatively. Brief use of sling may be used with return to stationary workouts almost immediately and road riding in 1 to 2 wk.
Radial head fractures
Radial head fractures are common from falls on an outstretched hand. Aspiration of hemarthrosis with infiltration of anesthesia helps with pain relief and evaluation for mechanical block. Early range of motion exercises should be encouraged to achieve full extension. Most athletes with nondisplaced fractures can return usually to riding in 1 to 2 wk.
Rib fractures are common from falls. Multiple rib fractures appear to occur more often in Masters cyclists with a higher rate of pneumothorax; chest tubes are required often. CT should be considered to evaluate for intra-abdominal trauma. Return to racing may take 4 to 6 wk.
Concussions in cycling historically have been managed differently from other contact-collision sports like football. In stage races like the Tour de France, a rider must finish the stage within a percentage of the stage winner’s time to continue racing. There are no time outs or substitutions, and the peloton waits for no one. A rider who crashes has to get back on his bike and “chase back on” drafting off team cars. On stage 1 of the 1996 Tour, Luc Leblanc crashed and lay on the side of the road motionless. He was put back on his bike when he regained consciousness. He went on to win Stage 7. A stage win in the Tour de France is a career-defining win for a cyclist, bigger than an Olympic medal.
It is common to this day to put a rider back in a race after a closed head injury as long as the rider is willing and able to ride. There is no Sideline Concussion Assessment Tool in cycling. Assessment on the side of the road is done rapidly as the race goes on, often by a mechanic or team director. If a rider can get up and mount his bike, he soldiers on. Slower reaction times and impaired speed of processing information are seen commonly in concussed athletes, and return of a cyclist who might be experiencing a concussion may place the athlete and the peloton at risk from further accidents. The risk of diffuse cerebral swelling after head injury, a rare occurrence seen more often in boxers and children, is unknown in cycling. The pathophysiology and risk of chronic traumatic encephalopathy, a neurodegenerative tauopathy, diagnosed in postmortem cases in other contact collision sports such as hockey and football, also are unknown as they relate to closed head injuries in cycling.
Helmets were made mandatory in professional cycling in 2003, 8 wk after the death of professional road cyclist Andre Kivilev, who sustained a skull fracture from a crash in Paris-Nice. Helmets have been shown to prevent skull fractures and intracranial hemorrhage (8). To date, there is no scientific evidence that they reduce the incidence of concussions. Bicycle helmets are designed to protect the head by reducing the rate at which the skull and brain are decelerated by an impact. The expanded polystyrene liner upon impact is designed to compress, dissipating the energy over a rapidly increasing area like a cone. After a blow to the head, a helmet should be discarded whether or not it appears broken.
Concussions in cycling should be handled as in other sports with recommendations from the Fourth International Consensus Conference on Concussion in Sport held in Zurich in 2012 (44). Any cyclist who is suspected of sustaining a concussion should be evaluated by a licensed health care provider on-site, and if no health care provider is available, the athlete should be removed from the sport, with urgent referral to a physician trained and experienced in management of concussions. Any cyclist diagnosed with a concussion should not be allowed to return to play on the day of the injury. The cornerstone of concussion symptom management is complete physical and cognitive rest until the acute symptoms resolve, although to date, there is no published scientific evidence evaluating the effect or duration of rest. Once asymptomatic, a stepwise graded return to play may be initiated, beginning with easy rides on a stationary trainer. Management and return to play should be guided ultimately by clinical judgment on an individual case basis. All cyclists, regardless of their level of participation, should be managed with the same paradigm.
Road rash is the most common crash injury and should be treated with rapid scrubbing and debridement with soap and water to prevent infection and staining (“tattooing”). Topical anesthetic should be used. Wounds should not be left uncovered; large scabs inhibit wound healing and inhibit range of motion required to pedal or hold the bars. Open wounds will stick painfully to bedding at night.
Wounds can be covered with semipermeable films, hydrocolloid dressings, or bioclusive bandages. Alternatively wounds may be covered with nonadherent dressings and antibiotic ointment with daily dressing changes and cleansing of exudates until pink healthy granulation tissue forms. Dressings are padded with gauze, wrapped in stretch gauze, and then covered in tube stretch gauze.
Contusions are equally common as road rash. The most common site is the quadriceps, from contact with pavement or collision with cars. Immediate placement of the knee in 120° of flexion for 24 h may allow an athlete to return to sports sooner (3). Scientific studies on the use of ice or nonsteroidal anti-inflammatory drugs in contusions are lacking. Localized hematomas or seromas, common from cycling contusions, can be visualized easily by ultrasound and are treated most effectively with aspiration. Aspirations often can exceed 200 mL and may require repeat treatments.
Pre-patella bursitis may be caused by direct blow from a crash or from repetition. If from a crash with road rash, have a high index of suspicion of infection; aspirate and send for culture and Gram stain. Most cyclists with bursitis can continue to train at modified intensity. Cortisone is for recalcitrant cases.
Intra-abdominal cavity contusions
Intra-abdominal trauma from crashes occur more often in children performing BMX stunts and in mountain biking. The cause is often blunt trauma from horizontal bar ends. In a retrospective review of children involved in cycling crashes admitted to a tertiary center over 5 years, 31 out of 196 (16%) sustained abdominal injuries with 19 major visceral injuries, seven requiring surgery. Over the same period, no child with head trauma required surgery (47). Alessandro Ballan, 2008 World Road Champion, had an emergency splenectomy performed in 2012 after a solo crash on a descent that fractured his femur and a rib, which punctured his lung and ruptured his spleen. Most intra-abdominal contusions are treated with serial observation and diagnostic imaging.
Overuse injuries (Table 2) are common in cycling but rarely require prolonged time off the bike. In a study of 108 professionals in 1 season, 58.3% experienced an overuse injury (15). In a study of 51 professionals over 4 seasons, 62.7% reported an overuse injury (19). In a study of 518 amateur cyclists, 85% experienced an overuse injury (68). Among overuse injuries in professionals, 64% required less than 7 d off from competition, 32% required 7 to 28 d off, and 4% required more than 28 d off (1 case of osteitis pubis and 1 case of iliac artery endofibrosis) (7).
The knee is the most common overuse injury site in the cyclist. Knee injuries account for 62% of all overuse injuries in professionals (7). Based on the location of pain, bicycle adjustments may be made (4) (Table 1). Ultrasound may help localize extraarticular pathology.
Lateral knee pain
Iliotibial band syndrome (ITBS) is the most common cause of lateral knee pain in cyclists. Historically regarded as a friction syndrome from a snapping iliotibial band (ITB) over the lateral femoral condyle, Fairclough et al. (24) argue that ITBS is not from snapping but from compression of fat beneath the ITB. In cadavers, the ITB was found anchored to the femur by fibrous strands, associated with innervated and vascularized fat containing Pacinian corpuscles, suggesting that ITBS is more of an enthesopathy. Some report found no bursal sacs (24,36,46). Others have treated ITBS with bursectomy (31). Some have removed surgically cyst-like structures, which are possible extensions of the lateral synovial capsule (17,48). Holmes et al. (34) reported fibrosis and chronic inflammatory changes on microscopic examination of excised ITB, while others question if any pathological change takes place in the ITB (24). The syndrome is likely a spectrum of different entities.
The causes of ITBS are rapid increase in intensity and mileage, pushing big gears, hills, windy conditions, time trialing, and positional causes such as toes pointing inward, excessive pedal float, or worn cleats. Weak hip abductors may be less of an issue in cyclists than in runners with ITBS since cyclists are seated in the saddle most of the time.
Bike fit treatments involve adjusting cleats, checking bike fit, and leg length evaluation with shims as needed. Physical therapy, stretching, foam rolling, and massage therapy are treatment options. Professional cycling teams employ Soigneurs for daily massage therapy. Manipulation of the pelvis should be performed for somatic dysfunctions, which commonly occur from crashes and are overlooked often. Cortisone injection may be considered. Under ultrasound guidance, injections may be directed at the tendon sheath, if tenosynovitis is present, or between the ITB and femoral condyle, if anechoic or hypoechoic echotexture is noted against the femoral condyle. Many cyclists with ITBS can recover while continuing to ride albeit at a lesser intensity and duration.
Surgery for recalcitrant cases has ranged from removal of an elliptical piece of the distal posterior band (34) to the “mesh technique” (57) to surgical lengthening or Z-plasty (6,55). Surgery on cyclists commonly seen in the past is never recommended by the author.
Biceps femoris tendinopathy presents with pain more posterior lateral than ITBS. Biceps femoris tendinopathy occurred equally as patella tendinopathy in professionals (19), although the author finds that it occurs much less. Massage therapy, eccentric strengthening, dynamic stretching, or a short time off the bike for severe cases are all treatment options.
Anterior knee pain
Anterior knee pain is the most common reason cyclists seek medical care. Anterior knee pain should not be lumped into one diagnosis of patellofemoral pain syndrome (PFPS) or chondromalacia.
Patella tendon pain may occur at the entheses of the tibia tubercle, midportion, or inferior pole of the patella and may be a strain, tear, or tendonosis (54). Pain can become chronic or recurrent. Common causes in cyclists are similar to ITBS and include pushing big gears, hills, windy conditions, rapidly increasing mileage or intensity, or a bicycle set-up with a saddle too low or forward, or with cranks too long. Time off the bike or limiting intensity and duration may be needed. Physical therapy, manual therapy, and massage are treatment options. Eccentric strength training is a popular home exercise program that may have a positive effect for patella tendinopathy (66). A usual program is twice-daily training with 3 sets of 15 repetitions for 12 wk, performed on a 25° decline board, with some level of discomfort, and cessation of sports activity. Almost all cyclists are unwilling to stop cycling for 12 wk. Sclerosing neovessels outside the tendon for painful chronic tendinopathy is a novel treatment that may challenge the need for surgery (2). Percutaneous tenotomy, prolotherapy, platelet-rich plasma therapy, and stem cell injection therapies are other emerging nonsurgical treatments also warranting more scientific research.
PFPS is a diagnosis of exclusion. An effusion indicates intraarticular pathology and warrants an MRI, or aspiration for fluid analysis. PFPS may be caused by a saddle too low or forward or from cranks too long. Cycling causes and treatments are similar to the patella tendon. A diagnosis of chondromalacia patella should be made only after arthroscopy, although it is not treated easily surgically. Barrios et al. (7) found chondromalacia in 10 out of 10 cyclists who underwent arthroscopy for recurrent pain.
Medial knee pain
The most common causes of medial knee pain in the cyclist are MCL bursitis, medial plica syndrome, pes anserine syndrome, and less commonly medial meniscus tear. Excessive float or no float in a pedal may contribute to medial knee pain. Bike fit evaluation, modification of training, physical and manual therapy, or injections are treatment options. Medial meniscus tears while not caused by pedaling can become symptomatic from twisting out of a pedal. Symptomatic meniscal tears may be treated with modification of activity, pedal tension adjustment, watchful waiting, injections, and even continued cycling prior to entertaining a meniscectomy. Caution should be noted if a cyclist has a tear on MRI; one should not assume it is the cause of pain.
Medial plica syndrome presents with pain and a snapping or clicking sensation anterior medial over the femoral condyle. A symptomatic thickened plica may be palpated over the medial condyle while the patient flexes and extends the knee. Diagnosis of a symptomatic plica is made by exclusion, and presence of a plica does not imply pathology. A plica may be seen on MRI, although a negative MRI does not rule out a symptomatic plica either. Treatments include cortisone injection, physical therapy, and modification of training prior to surgery. Rapid return to cycling after surgical excision is usual.
Proximal ITBS or Greater Trochanteric Pain Syndrome
Proximal ITBS, lateral “hip” pain and tenderness over the greater trochanter, is not as common in cyclists as ITBS at the knee. The athlete is misdiagnosed often with trochanteric bursitis. With ultrasound and MRI, we now know that bursitis is rarely present (33,35). One histopathological study failed to find any evidence of acute or chronic inflammation in bursal specimens from patients diagnosed with bursitis; pathological specimens contained mostly fibroadipose tissue (62). In an MRI study on women with “trochanteric bursitis,” 45.8% had a gluteus medius tear, 62.5% had gluteus medius tendonitis, and 8% had bursitis (9). Some authors contend gluteal tendinopathy is similar to rotator cuff pathogenesis, with reactive secondary bursitis similar to subacromial bursitis (38). Pathology may include a spectrum of entities such as tendonosis, partial tears, complete tears, undersurface tears, and tears with retraction, with the gluteus medius tendon most commonly involved. Dynamic ultrasound of “external hip snapping” has documented snapping of the ITB over the greater trochanter with a hypoechoic and thickened ITB (16). Whether the source of the pain is the tensor fascia lata or ITB is unclear.
There are no specific studies involving cyclists (seated athletes), where the mechanism of injury appears different from those who are studied more often such as runners or older nonathletes. The etiology of lateral “hip” pain in the cyclist may be similar to the theory of ITBS at the knee with compression of underlying tissue against the greater trochanter. It can mimic pain from a lumbar disc or tumor, which often causes posterior thigh or buttock pain, or osteoarthritis of the hip, which should cause groin pain.
The cause usually is riding excessive mileage. Backing off and massage will quickly cure most of these cases. Improper bike fit may reveal “hip rocking” when pedaling with a high saddle. Recommend treatment includes bike fit adjustment, physical therapy, manipulation, or cortisone injection. Historically injections are directed at the point of maximal tenderness. With ultrasound guidance, the injection may be directed at any tendonosis, tear, or bursitis. A 2- to 3-inch needle, longer than one would expect, is required often to reach the gluteal entheses at the greater trochanter or deeper bursal structures. There are no known clinical studies comparing outcomes of ultrasound-guided injections versus blind technique for the treatment of greater trochanteric pain syndrome. In a randomized clinical control comparison of fluoroscopic guided injection versus blind injection, there were no differences in outcomes favoring either group (13).
Laurent Fignon (26), a Tour De France champion famous for his 8-s loss to Greg LeMond, developed an injury to his Achilles at the age of 24 years, blamed on a “stupid knock from the pedal.” Fignon ultimately required surgery for a nodule and partial tear. In a 4-year study of 51 professional cyclists, 5 cases of Achilles tendinopathy were reported compared with 3 cases of patella and 8 cases of ITB tendinopathy (19). Achilles tendinopathy may occur from riding “too much too soon,” improper pedaling technique, or improper bike fit. Excessive plantarflexion at BDC from too high a saddle may cause strain. Francis reported that the optimum plantarflexion in BDC pedal position should be approximately 13°, which corresponds to about 20° plantarflexion from the horizontal (20,27). Excessive dorsiflexion at BDC from a low saddle or pushing the heel down in an attempt to generate more power also may cause strain of the Achilles (20). Physical therapy, manual therapy, and eccentric strengthening are treatment options for Achilles tendinopathy.
The following is a brief description of pedal stroke, which is pertinent but beyond the scope of the article. The pedal stroke may be broken down into the downward propulsive phase and upward relaxation phase. Simple observation of cyclists (whether or not they are using clipless pedal systems) reveals that a rider’s heel lowers during the downstroke (ankle dorsiflexes) and a rider’s heel raises during the upstroke (ankle plantar flexes), mostly due to lower limb movement and the biomechanics of cycling with a rotating pedal spindle on a moving crank. This ankle range of motion appears within a narrow range of 24° (23). If the saddle height is set correctly, then the heel should not drop below horizontal on the downstroke.
“Ankling,” purposely pressing the heel down at the start of the downward pedal stroke to a point below the horizontal and then lifting the heel up on the up stroke (the technique used originally on High-wheelers with short cranks), recently has been found to be significantly less efficient than normal pedaling (70) and likely contributes to ankle tendon problems. The mean range of motion during ankling is 46.4° versus 27.9° without ankling, with a maximum of 65.2° versus 37.6° and a minimum of 25.3° versus 14.3° (70). Although most cyclists believe they should pull up on the pedals while cycling, studies on U.S. national team cyclists have shown that even on the upstroke, vector forces are downward on the pedal (the leg moving upwards in the relaxation phase is lifted actually by the leg moving downward) (11,25). The leg cannot be pulled actively up faster and harder in the upstroke than the leg pushing down in the downstroke. It is the maximal torque during the downstroke that separates the elite from recreational cyclists (10).
Iliac Artery Endofibrosis and Kinking
Flow limitations in iliac arteries have been reported mostly in cyclists likely from riding position, although cases exist in speed skaters, runners, soccer players, and cross-country skiers. Flow limitations may be from kinking (functional iliac artery obstruction) or endofibrosis (external iliac artery endofibrosis) (51). Schep et al. (58) estimates the prevalence to be 10% to 20% among elite and professionals. A rider often sees multiple physicians with comprehensive orthopedic and neurological work ups prior to diagnosis. The cyclist may report a sensation of dead leg, lack of power, cramp, or pain in the leg worse with steady exertion such as climbing or time trialing. A detailed questionnaire helps differentiate vascular from nonvascular causes. Physical examination is usually normal, although a bruit in the inguinal region may be heard, more often postexercise. A reliable, reproducible imaging modality does not exist. A flow chart guiding investigation and management exists (51). Initial test is a provocative ankle brachial index and duplex ultrasound, immediately postcycling with the hip and knee flexed. Magnetic resonance angiography may assess vessel length or kinking, and digital subtraction angiography may identify tethering of arterial branches. CT angiography also has been used.
There are multiple treatment options. Arterial release is performed if stenosis is less than 15%, and artery is not lengthened. Vessel shortening with endofibrosectomy is performed for a lengthened vessel. Endofibrosectomy and patch angioplasty, or interpositional grafting, are performed for intravascular lesions. Complete resection and replacement with a saphenous vein or synthetic graft have been performed also. Angioplasty or endoluminal stent placement is not recommended (51).
Professionals have returned to racing postsurgery, although no long-term outcomes exist. Ryan Cox, a 28-year-old professional, died 3 wk after surgery when his artery ruptured. Conservative treatment in recreational cyclists include a change in position to one of less hip flexion or cessation of sport.
Injuries in cycling occur at a high rate from bicycle contact, traumatic events, and overuse. Overuse ailments occur primarily in the knee. Traumatic lesions occur primarily in the shoulder region. Many bicycle contact and overuse ailments are relieved with bike fit adjustments. Overuse injuries are treated successfully with massage, physical therapy, and modification of training. Most injured cyclists are able and willing to train and even race while injured. More evidence-based research on injuries in cycling is needed.
The author thanks Kaitlin Anders, MS, ATC, for helping with the compilation of data and creation of the tables.
The author declares no conflict of interests and does not have any financial disclosures.
1. Ackery AD, McLellan BA, Redelmeier DA. Bicyclist deaths and striking vehicles in the USA. Inj. Prev.
2012; 18: 22–6.
2. Alfredson H, Ohberg L. Neovascularisation in chronic painful patellar tendinosis — promising results after sclerosing neovessels outside the tendon challenge the need for surgery. Knee Surg. Sports Traumatol. Arthrosc.
2005; 13: 74–80.
3. Aronen JG, Garrick JG, Chronister RD, McDevitt ER. Quadriceps contusions: clinical results of immediate immobilization in 120 degrees of knee flexion. Clin. J. Sport Med.
2006; 16: 383–7.
4. Asplund C, St Pierre P. Knee pain and bicycling. Phys. Sportsmed.
2004; 32: 1–11.
5. Baker A. Traumatic bicycle injuries in a Masters club. Traum. Inj.
2003; 200: 1–8.
6. Barber FA, Boothby MH, Troop RL. Z-plasty lengthening for iliotibial band friction syndrome. J. Knee Surg.
2007; 20: 281–4.
7. Barrios C, Sala D, Terrados N, Valenti JR. Traumatic and overuse injuries in elite professional cyclists. Sports Exerc. Inj.
1997; 3: 176–9.
8. Bergenstal J, Davis SM, Sikora R, Paulson D, Whiteman C. Pediatric bicycle injury prevention and the effect of helmet use: the West Virginia experience. W. V. Med. J.
2012; 108: 78–81.
9. Bird PA, Oakley SP, Shnier R, Krikham BW. Prospective evaluation of magnetic resonance imaging and physical examination findings in patients with greater trochanteric pain syndrome. Arthritis Rheum.
2001; 44: 2138–45.
10. Broker JP. Cycling biomechanics: road and mountain. In: Burke ER, editor. High Tech Cycling
. Champaign (IL): Human Kinetics; 2003. p. 123–38.
11. Broker JP, Gregor RJ. Cycling biomechanics. In: Burke ER, editor. High Tech Cycling
. Champaign (IL): Human Kinetics, 1996, p. 145–6.
12. Cohen JD, Gross MT. Effect of bicycle racing saddle design on transcutaneous penile oxygen pressure. J. Sports Med. Phys. Fitness
. 2005; 45: 409–18.
13. Cohen SP, Strassles SA, Foster L, et al. Comparison of fluoroscopically guided and blind corticosteroid injections for greater trochanteric pain syndrome: multicentre randomised controlled trial. BMJ
. 2009; 338: b10088.
14. Conn JM, Annest JL, Gilchrist J. Sports and recreational related injury episodes in the US population, 1997–1999. Inj. Prev.
2003; 9: 117–23.
15. Clarsen B, Krosshaug T, Bahr R. Overuse injuries in professional road cyclists. Am. J. Sports Med.
2010; 38: 2494–501.
16. Choi Y, Lee S, Song B, et al. Dynamic sonography of external snapping hip syndrome. J. Ultrasound Med.
2002; 21: 753–8.
17. Costa ML, Marshall T, Donell ST, Phillips H. Knee synovial cyst presenting as iliotibial band friction syndrome. Knee
. 2004; 3: 247–8.
18. Dannenberg AL, Needle S, Mullady D, Kolodner K. Predictors of injury a month 1638 riders in a recreational long-distance bicycle tour: cycle across Maryland. Am. J. Sports Med.
1996; 24: 747–53.
19. De Bernardo N, Barrios C, Vera P, Laíz C, Hadala M. Incidence and risk for traumatic an overuse injuries in top-level road cyclists. J. Sports Sci.
2012; 30: 1047–53.
20. De Vey Mestdagh K. Personal perspective: in search of an optimum cycling posture. Appl. Ergon.
1998; 29: 325–34.
21. Dettori JR, Koepsell TD, Cummings P, Corman JM. Erectile dysfunction after a long-distance cycling event: associations with bicycle characteristics. J. Urol.
2004; 172: 637–41.
22. Duan X, Zhong G, Cen S, Huang F, Xiang Z. Plating versus intramedullary pin or conservative treatment for midshaft fracture of clavicle: a meta-analysis of randomized controlled trials. J. Shoulder Elbow Surg.
2011; 20: 1008–15.
23. Ericson MO, Nisell R, Nemeth G. Joint motions of the lower limb during ergometer cycling. J. Orthop. Sports Phys. Ther.
1988; 9: 273–8.
24. Fairclough J, Hayashi K, Toumi H, et al. The functional anatomy of the iliotibial band during flexion and extension of the knee: implications for understanding iliotibial band syndrome. J. Anat.
2006; 208: 309–16.
25. Faria IE, Cavanagh PR. The Physiology and Biomechanics of Cycling
. New York: Wiley, 1978.
26. Fignon L. We were Young and Carefree
. Yellow Jersey Press, 2010, p. 143–6.
27. Francis PR. ‘Injury prevention for cyclists: a biomechanical approach’ in Burke ER. Science of Cycling
. Champaign (IL): Human Kinetics Publishers, 1986, p. 145–84.
28. González-Pérez R, Carnero L, Arbide N, Soloeta R. Perineal nodular induration in cyclists. Actas Dermosifiliogr.
2009; 100: 907–22.
29. Greve MW, Modabber MR. An epidemic of traumatic brain injury in professional cycling: a call to action. Clin. J. Sport Med.
2012; 22: 81–2.
30. Hankey G, Gubbay SS. Compressive mononeuropathy of the deep palmar branch of the ulnar nerve in cyclists. J. Neurol. Neurosurg. Psychiatry
. 1988; 51: 1588–90.
31. Hariri S, Savidge ET, Reinold MM, Zachazewski J, Gill TJ. Treatment of recalcitrant iliotibial band friction syndrome with open iliotibial band bursectomy: indications, technique, and clinical outcomes. Am J. Sports Med.
2009; 37: 1417–24.
32. Hill JM, McGuire MH, Crosby LA. Closed treatment of displaced middle-third fractures of the clavicle gives poor results. J. Bone Joint Surg. Br.
1997; 79: 537–9.
33. Ho GWK, Howard TM. Greater trochanteric pain syndrome: more than bursitis and iliotibial tract friction. Am. J. Sports Med.
2012; 11: 232–8.
34. Holmes JC, Pruitt AL, Whalen NJ. Iliotibial band syndrome in cyclists. Am. J. Sports Med.
1993; 21: 419–24.
36. Isusi M, Oleaga L, Campo M, Grande D. MRI findings in iliotibial band friction syndrome: a report of two cases. Radiologia.
2007; 6: 433–5.
37. Johnson JE, Johnson KA, Unni KK. Persistent pain after excision of interdigital neuroma. J. Bone Joint Surg. Am.
1988; 70-A: 651–7. No. 5.
38. Kingzett-Taylor A, Tirman PFJ, Feller J, et al. Tendinosis and tears of gluteus medius and minimus muscles as a cause of hip pain: MR imaging findings. AJR
. 1999; 173: 1123–6.
39. Kulund D, Brubaker C. Injuries in the Bikecentennial Tour. Physician Sports Med.
40. Lee KT, Kim JB, Young KW, et al. Long-term results of neurectomy in the treatment of Morton’s neuroma: more than 10 years’ follow-up. Foot Ankle Spec.
2011; 4: 349–53.
41. Leibovitch I, Mor Y. The vicious cycling: bicycling related urogenital disorders. Eur. Urol.
2005; 47: 277–87.
42. Maimaris C, Zadeh HG. Ulnar nerve compression in the cyclist’s hand: two case reports and review of the literature. Br. J. Sports Med.
1990; 24: 245–6.
43. Mann RA, Reynolds JC. Interdigital neuroma — a critical clinical analysis. Foot Ankle.
1983; 3: 238–43.
44. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Br. J. Sports Med.
2013; 47: 250–8.
45. Megan J, Patterson M, Jaggars M, Boyer M. Ulnar and median nerve palsy in long-distance cyclists, a prospective study. Am. J. Sports Med.
2003; 31: 585–9.
46. Muhle C, Ahn J, Yeh L, et al. Iliotibial band friction syndrome: MR imaging findings in 16 patients and MR arthrographic study of six cadaveric knees. Radiology
. 1999; 212: 103–10.
47. Muthucumaru M, Keys C, Kimber C, et al. Trend of severe abdominal injuries from bicycle accidents in children: a preventable condition. J. Paediatr. Child Health
. 2012; 48: 259–62.
48. Nemeth WC, Sanders BL. The lateral synovial recess of the knee: anatomy and role in chronic iliotibial band friction syndrome. Arthroscopy
. 1996; 12: 574–80.
49. Nowak J, Holgersson M, Larsson S. Sequelae from clavicular fractures are common: a prospective study of 222 patients. Acta Orthop.
2005; 76: 496–502.
50. Pace A, Scammell B, Dhar S. The outcome of Morton’s neurectomy in the treatment of metatarsalgia. Int. Orthop.
2010; 34: 511–5.
51. Peach G, Schep G, Palfreeman R, et al. Endofibrosis and kinking of the iliac arteries in athletes: a systemic review. Eur. J. Vasc. Endovasc. Surg.
52. Pfeiffer RP, Kronisch RL. Off-road cycling injuries. An overview. Sports Med.
1995; 19: 311–25.
53. Potter JM, Jones C, Wild LM, Schemitsch EH, McKee MD. Does delay matter? The restoration of objectively measured shoulder strength and patient-oriented outcome after immediate fixation versus delayed reconstruction of displaced midshaft fractures of the clavicle. J. Shoulder Elbow Surg.
2007; 16: 514–8.
54. Rees JD, Houghton J, Srikanthan A, West A. The location of pathology in patellar tendinopathy. Br. J. Sports Med.
2013; 47: 9 e2.
55. Richards DP, Alan Barber F, Troop RL. Iliotibial band Z-lengthening. Arthroscopy
. 2003; 19: 326–9.
56. Romanow NTR, Couperthwaite AB, McCormack GR, et al. Environmental determinants of bicycling injuries in Alberta, Canada. J. Environ. Public Health
. 2012; 2012: 1–12.
57. Sangkaew C. Surgical treatment of iliotibial band friction syndrome with the mesh techniques. Arch. Orthop. Trauma Surg.
2007; 127: 303–6.
58. Schep G, Schmikli SL, Bender MH, et al. Recognising vascular causes of leg complains in endurance athletes. Part 1: validation of a decision algorithm. Int. J. Sports Med.
2002; 23: 313–21.
59. Schrader SM, Breitenstein MJ, Clark JC, Lowe BD, Turner TW. Nocturnal penile tumescence and rigidity in bicycling patrol officers. J. Androl.
2002; 23: 927–34.
60. Schwarzer U, Sommer F, Klotz T, Cremer C, Engelmann U. Cycling and penile oxygen pressure: the type of saddle matters. Eur. Urol.
2002; 41: 139–43.
61. Silberman MR, Webner D, Collina S, Shiple BJ. Road bicycle fit. Clin. J. Sport Med.
2005; 15: 269–74.
62. Silva F, Adams T, Feinstein J, Arroyo RA. Trochanteric bursitis: refuting the myth of inflammation. J. Clin. Rheumatol.
2008; 14: 82–6.
63. Sommer F, Konig D, Graft C, Schwarzer U, Bertram C, Klotz T, et al. Impotence and genital numbness in cyclists. Int. J. Sports Med.
2001; 22: 410–3.
64. Tan V, Seldes RM, Daluiski A. In-line skating injuries. Sports Med.
2001; 31: 691–9.
65. Thomsom CE, Gibson JN, Martin D. Interventions for the treatment of Morton’s neuroma. Cochrane Database Syst. Rev.
66. Visnes H, Bahr R. The evolution of eccentric training as treatment for patella tendinopathy (jumper’s knee): a critical review of exercise programmes. Br. J. Sports Med.
2007; 41: 217–23.
67. Weiss B. Nontraumatic injuries in amateur long distance bicyclists. Am. J. Sports Med.
1985; 13: 187–92.
68. Wilber CA, Holland GJ, Madison RE, Loy SF. An epidemiological analysis of overuse injuries among recreational cyclists. Int. J. Sports Med.
1995; 16: 201–6.
69. Younger ASE, Claridge RJ. The role of diagnostic block in the management of Morton’s neuroma. Can. J. Surg.
1998; 41: 127–30.
70. Zommers A. Variations in pedaling technique of competitive cyclists: the effect on biological efficiency [dissertation]
. Victoria University of Technology; 2000. http://vuir.vu.edu.au/15742/