Eccentric Hamstring Strength Imbalance among Football and Soccer Athletes.

OBJECTIVES: Hamstring strain injuries (HSI) are common among football and soccer athletes. Eccentric strength imbalance is considered a contributing factor for HSI. There is, however, a paucity of data on hamstring imbalances of soccer and American football athletes as they age and advance in skill level. High school athletes will display greater interlimb discrepancies compared with collegiate and professional athletes. In addition, soccer athletes will exhibit greater hamstring asymmetry than American football athletes. METHODS: Hamstring testing was performed on soccer and American football athletes using the NordBord Hamstring Testing System (Vald Performance, Albion, Australia). Age, sex, weight, sport specialization, and sport level were recorded. Maximum hamstring forces (N), torque (N · m), and work (N · s) were measured. Hamstring imbalance (%) was calculated by dividing the absolute value of the difference in leg forces divided by their sum. One-way analysis of variance and independent sample t tests compared measurements between athlete groups. RESULTS: A total of 631 athletes completed measurements, including 88 high school male soccer, 25 college male soccer, 23 professional male soccer, 83 high school female soccer, 28 college female soccer, 288 high school football, and 96 college football athletes. High school soccer players displayed significantly greater imbalances for torque (P = 0.03) and work (P < 0.01) than football athletes. Imbalances for maximum force (P = 0.035), torque (P = 0.018), and work (P = 0.033) were significantly higher for male soccer athletes in high school compared with college- and professional-level athletes. Female high school soccer players had significantly higher imbalance in torque (P = 0.045) and work (P = 0.001) compared with female collegiate soccer players. Football athletes did not experience significant changes in force imbalances between skill levels. CONCLUSIONS: High school soccer athletes exhibit greater hamstring imbalances than football athletes. Higher levels of play in soccer, for both male and female athletes, correlate with less hamstring asymmetry.

Analysis of novel domain-specific mutations in the zebrafish ndr2/cyclops gene generated using CRISPR-Cas9 RNPs.

Nodal-related protein (ndr2) is amember of the transforming growth factor type ß superfamily of factors and is required for ventral midline patterning of the embryonic central nervous system in zebrafish. In humans, mutations in the gene encoding nodal cause holoprosencephaly and heterotaxy. Mutations in the ndr2 gene in the zebrafish (Danio rerio) lead to similar phenotypes, including loss of the medial floor plate, severe deficits in ventral forebrain development and cyclopia. Alleles of the ndr2 gene have been useful in studying patterning of ventral structures of the central nervous system. Fifteen different ndr2 alleles have been reported in zebrafish, of which eight were generated using chemical mutagenesis, four were radiation-induced and the remaining alleles were obtained via random insertion, gene targeting (TALEN) or unknown methods. Therefore, most mutation sites were random and could not be predicted a priori. Using the CRISPR-Cas9 system from Streptococcus pyogenes, we targeted distinct regions in all three exons of zebrafish ndr2 and observed cyclopia in the injected (G0) embryos.We show that the use of sgRNA-Cas9 ribonucleoprotein (RNP) complexes can cause penetrant cyclopic phenotypes in injected (G0) embryos. Targeted polymerase chain reaction amplicon analysis using Sanger sequencing showed that most of the alleles had small indels resulting in frameshifts. The sequence information correlates with the loss of ndr2 activity. In this study, we validate multiple CRISPR targets using an in vitro nuclease assay and in vivo analysis using embryos. We describe one specific mutant allele resulting in the loss of conserved terminal cysteine-coding sequences. This study is another demonstration of the utility of the CRISPR-Cas9 system in generating domain-specific mutations and provides further insights into the structure-function of the ndr2 gene.