The most common areas for injury in the club and collegiate female gymnast (1) in order of frequency are (a) the ankle, (b) the wrist, and (c) the spine. Brüggemann, the current President of the Scientific Commission of the Federation of International Gymnastics, recorded that at takeoff for gymnastic tumbling on a spring floor (roundoff to a back-tuck somersault), the resultant moments at the ankle joint were 310 N·m in the sagittal plane and 100 N·m in the frontal plane (2). This correlates to an Achilles tendon force of 7,500 N (˜15 times the gymnast’s body weight), a tibiotalar joint force of 11,000 N (˜23 times body weight) and a talonavicular joint force of 8,000 N (˜15 times body weight). These forces in the foot and ankle are almost doubled with improper foot eversion or pronation by decreasing the contact area of the joint surfaces. With these types of extreme forces, the likelihood of injury of the foot and ankle is high.

Current elite-level female gymnasts are reported to have an 11.1% incidence of spondylolysis and a 2.9% incidence of spondylolisthesis (2). These statistics do not significantly differ from the normal population, yet a 44.4% incidence of osteochondritic changes was found in female gymnasts. The majority of these changes were end-plate compression fractures, where the nucleus pulposus herniates into the vertebral body. In the immature spine, especially during the adolescent growth spurt, the disc is stronger than the cartilaginous end plate. Thus, the end plate becomes damaged before the disc when exposed to compressive forces. These fractures are mainly found in the thoracolumbar junction (T11-L3). This area of the spine is at high risk for fracture due to its relative neutral alignment and transition between the more rigid thoracic spine and more flexible lumbar spine (1).

Swärd et al. found that normal disc heights were present with first diagnosis of vertebral end-plate damage in the gymnast. However, subsequent follow-up revealed marked disc
degeneration 10 to 12 months after injury (3). Nassar and co-workers studied the 1999 USA Gymnastics Female Artistic National Team, and 11 of 19 gymnasts (58%) had lumbar disc degeneration on magnetic resonance imaging (MRI). Anterior apophyseal ring fractures were found in 7 of 19 gymnasts (37%) (4).

The skills and equipment in gymnastics have changed over the years, so findings in older studies on gymnasts are outdated and of little value. In the past, gymnasts performed many back walkovers, front walkovers, limbers, and other skills that created exceptional stress to the lumbothoracic spine. These skills are no longer performed with the same frequency as in the past. Gymnastic coaches have improved their technique with emphasis on proper use of the shoulders and thoracic spine to remove stress from the lower lumbar pars interarticularis. The addition of new training aids such as sting mats can reduce tumbling impact forces on the spine by 20% (2). Finally, reduction in the incidence of posterior column fractures may be attributed to coaches’ and athletes’ awareness to seek medical help early on for these injuries when only a stress reaction may be present and before a full stress fracture occurs.

The high-impact landing forces in gymnastics can be tolerated by the gymnast only by appropriate timing and balance of the muscular activity of the spine and lower extremity to distribute these forces most efficiently through the spine. If the gymnast performs a routine with improper timing or muscular firing sequence, the potential for injury on landing becomes great. Landing with a flexed trunk increases the pressure on the anterior end plates most significantly at the thoracolumbar junction. This leads to end-plate damage and marked disc degeneration noted 10 to 12 months after injury (3).

Hall states that the main cause of low back pain in the female artistic gymnast is uncontrollable hyperextension of the lumbar spine (5). Brady showed that a decrease in hip extension and poor thoracic extension motion contribute significantly to low back pain (6). Jull and Janda coined the term pelvic crossed syndrome (7) to explain how a gradual-onset nontraumatic overuse injury may develop in accordance with the explanations of gymnast lumbar mechanics given by Hall and Brady.

Pelvic crossed syndrome is an imbalance in the lumbar-pelvic-hip complex whereby the short and tight hip flexors and lumbar erector spinae muscles neurologically inhibit the proper firing and strength of the abdominal and gluteal muscles (7). This arrangement enhances an anterior pelvic tilt, increases lumbar lordosis, and shortens the hip flexors. The thoracolumbar erector spinae and hamstrings compensate by increasing activity, which creates hip extension.

The syndrome continues with gluteus medius weakness, which causes compensatory increased activity in the ipsilateral iliotibial band, tensor fasciae latae, and quadratus lumborum. The abdominal muscles display weakness with increased iliopsoas muscle activity, which increases trunk flexion. Sherrington’s law of reciprocal innervation has been proposed to explain this muscle inhibition. This type of muscle imbalance is self-sustaining without appropriate therapeutic intervention (8). When the inhibited muscle is exercised to create a maximal contraction, the electromyographic activity of the muscle actually decreases. No matter how specific the method of strengthening is, the muscle imbalance pattern is only reinforced unless the hypertonic/shortened muscle is first stretched (8).

Optimal function of the pelvis is vital to allow for the extreme range of motion, power, and balance needed to perform artistic gymnastics. The pelvis is the major connection between the upper and lower extremities; therefore, the pelvis should be evaluated for dysfunction with a large variety of injuries, such as ankle, shin, quadriceps, hip flexor, hip adductor, iliotibial band, gluteal region, pelvic bones, abdominal musculature, spine, and shoulder complex.