Low-intensity pulsed ultrasound (LIPUS) has been proved to promote the proliferation of myoblast C2C12. However, whether LIPUS can effectively prevent muscle atrophy has not been clarified, and if so, what is the possible mechanism. The aim of this study is to evaluate the effects of LIPUS on muscle atrophy in hindlimb unloading rats, and explore the mechanisms. The rats were randomly divided into four groups: normal control group (NC), hindlimb unloading group (UL), hindlimb unloading plus 30 mW/cm² LIPUS irradiation group (UL + 30 mW/cm²), hindlimb unloading plus 80 mW/cm² LIPUS irradiation group (UL + 80 mW/cm²). The tails of rats in hindlimb unloading group were suspended for 28 days. The rats in the LIPUS treated group were simultaneously irradiated with LIPUS on gastrocnemius muscle in both lower legs at the sound intensity of 30 mW/cm² or 80 mW/cm² for 20 min/d for 28 days. C2C12 cells were exposed to LIPUS at 30 or 80 mW/cm² for 5 days. The results showed that LIPUS significantly promoted the proliferation and differentiation of myoblast C2C12, and prevented the decrease of cross-sectional area of muscle fiber and gastrocnemius mass in hindlimb unloading rats. LIPUS also significantly down regulated the expression of MSTN and its receptors ActRIIB, and up-regulated the expression of Akt and mTOR in gastrocnemius muscle of hindlimb unloading rats. In addition, three metabolic pathways (phenylalanine, tyrosine and tryptophan biosynthesis; alanine, aspartate and glutamate metabolism; glycine, serine and threonine metabolism) were selected as important metabolic pathways for hindlimb unloading effect. However, LIPUS promoted the stability of alanine, aspartate and glutamate metabolism pathway. These results suggest that the key mechanism of LIPUS in preventing muscle atrophy induced by hindlimb unloading may be related to promoting protein synthesis through MSTN/Akt/mTOR signaling pathway and stabilizing alanine, aspartate and glutamate metabolism.

This study aimed to assess the associations between sprint force–velocity profile variables with change of direction (COD) performance and to investigate the impact of these variables on asymmetries in COD speed performance. Ninety-nine participants (volleyball players: n = 44, basketball players: n = 55) performed 40 m sprints for Fv relationship calculation, two COD tests (Modified Agility T-test and 505 test). A partial least squares (PLS) regression analysis was conducted to determine the relationships between the variables. The V₀ was the most influential variable; it was negatively associated with COD performance variables (β = −0.260, −0.263 and −0.244 for MAT, 505-D and 505-ND, respectively), and F₀ (β = 0.169, 0.163) was associated with the COD performance variables (COD deficit D and COD deficit ND, respectively), slightly larger than the effects of Fv_slope (β = −0.162, −0.146), D_RF (β = −0.159, −0.142) and P_max (β = −0.162, −0.146). For COD deficit imbalance, the D_RF (β = −0.070) was the most influential variable followed by Fv_slope (β = −0.068), F₀ (β = 0.046) and gender (β = 0.031). V₀ and RF_max were the critical variables for improving COD performance that includes linear sprints, while D_RF, Fv_slope, F₀ and P_max collectively influence 180° COD performance. Meanwhile, D_RF and Fv_slope were important factors for asymmetries in COD speed performance. It is recommended to use the Fv profile to diagnose different COD movement patterns and then develop training plans accordingly for team sports played on smaller courts, such as basketball and volleyball.

Objectives: The aim of this study was to assess the relationship between variant loci significantly associated with sports-related traits in the GWAS Catalog database and sprint/power athlete status, as well as to explore the polygenic profile of elite athletes. Methods: Next-generation sequencing and microarray technology were used to genotype samples from 211 elite athletes who had achieved success in national or international competitions in power-based sports and from 522 non-athletes, who were healthy university students with no history of professional sports training. Variant loci collected from databases were extracted after imputation. Subsequently, 80% of the samples were randomly selected as the training set, and the remaining 20% as the validation set. Results: Association analysis of variant loci was conducted in the training set, and individual Total Genotype Score (TGS) were calculated using genotype dosage and lnOR, followed by the establishment of a logistic model, with predictive performance evaluated in the validation set. Association analysis was performed on 2075 variant loci, and after removing linked loci (r² > 0.2), 118 Tag SNPs (p ≤ 0.05) were identified. A logistic model built using 30 Tag SNPs (p ≤ 0.01) showed better performance in the validation set (AUC = 0.707). Conclusions: Our study identified 30 new genetic molecular markers and demonstrated that elite sprint/power athlete status is polygenic.