Background: Female athletes participating in high-risk sports suffer anterior cruciate ligament injury at a 4-to 6-fold greater rate than do male athletes.

To prospectively evaluate the effect of neuromuscular training on the incidence of knee injury in female athletes, we monitored two groups of female athletes, one trained before sports participation and the other not trained, and a group of untrained male athletes throughout the high school soccer, volleyball, and basketball seasons. Weekly reports included the number of practice and competition exposures and mechanism of injury. There were 14 serious knee injuries in the 1263 athletes tracked through the study. Ten of 463 untrained female athletes sustained serious knee injuries (8 noncontact), 2 of 366 trained female athletes sustained serious knee injuries (0 noncontact), and 2 of 434 male athletes sustained serious knee injuries (1 noncontact). The knee injury incidence per 1000 athlete-exposures was 0.43 in untrained female athletes, 0.12 in trained female athletes, and 0.09 in male athletes (P = 0.02, chi-square analysis). Untrained female athletes had a 3.6 times higher incidence of knee injury than trained female athletes (P = 0.05) and 4.8 times higher than male athletes (P = 0.03). The incidence of knee injury in trained female athletes was not significantly different from that in untrained male athletes (P = 0.86). The difference in the incidence of noncontact injuries between the female groups was also significant (P = 0.01). This prospective study demonstrated a decreased incidence of knee injury in female athletes after a specific plyometric training program.

Background-Athletes who return to sport participation after anterior cruciate ligament reconstruction (ACLR) have a higher risk of a second anterior cruciate ligament injury (either reinjury or contralateral injury) compared with non-anterior cruciate ligament-injured athletes.

Preventive programs to enhance knee control should focus on avoiding valgus motion and include distractions resembling those seen in match situations.

The absence of dynamic knee joint stability may be responsible for increased rates of knee injury in females but is not normally measured in athletes before participation. No method for accurate and practical screening and identification of athletes at increased risk of ACL injury is currently available to target those individuals that would benefit from neuromuscular training before sports participation. Prevention of female ACL injury from five times to equal the rate of males would allow tens of thousands of young females to avoid the potentially devastating effects of ACL injury on their athletic careers.

The mechanism underlying gender disparity in anterior cruciate ligament injury risk is likely multifactorial in nature. Several theories have been proposed to explain the mechanisms underlying the gender difference in anterior cruciate ligament injury rates. These theories include the intrinsic variables of anatomical, hormonal, neuromuscular, and biomechanical differences between genders and extrinsic variables. Identification of both extrinsic and intrinsic risk factors associated with the anterior cruciate ligament injury mechanism may provide direction for targeted prophylactic treatment to high-risk individuals.

Factors related to core stability predicted risk of athletic knee, ligament, and ACL injuries with high sensitivity and moderate specificity in female, but not male, athletes.

Members of the mitogen-activated protein kinase (MAPK) cascade such as extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 are implicated as important regulators of cardiomyocyte hypertrophic growth in culture. However, the role that individual MAPK pathways play in vivo has not been extensively evaluated. Here we generated nine transgenic mouse lines with cardiac-restricted expression of an activated MEK1 cDNA in the heart. MEK1 transgenic mice demonstrated concentric hypertrophy without signs of cardiomyopathy or lethality up to 12 months of age. MEK1 transgenic mice showed a dramatic increase in cardiac function, as measured by echocardiography and isolated working heart preparation, without signs of decompensation over time. MEK1 transgenic mice and MEK1 adenovirus-infected neonatal cardiomyocytes each demonstrated ERK1/2, but not p38 or JNK, activation. MEK1 transgenic mice and MEK1 adenovirus-infected cultured cardiomyocytes were also partially resistant to apoptotic stimuli. The results of the present study indicate that the MEK1-ERK1/2 signaling pathway stimulates a physiologic hypertrophy response associated with augmented cardiac function and partial resistance to apoptotsis.