The quadriceps angle, knowns as the Q-angle, is an anatomical feature of the human body that is still largely unknown and unstudied despite its initial discovery in the 1950s. The strength disparities between male and female athletes are largely determined by the Q-angle. In spite of a growing number of women participating in sports such as track, tennis, soccer, gymnastics, basketball, volleyball, swimming, and softball, studies investigating injuries in this group are scanty. Even though the Q-angle has been the subject of many studies carried out all over the world, a review of the literature regarding its effects on health and injury risk in female athletes has not yet been completed. The aim of this review is to examine the crucial role of the Q-angle in the biomechanics of the knee joint and its effect on performance and injury risk, particularly in female athletes. Furthermore, we highlight the greater likelihood of knee-related injuries seen in female athletes being caused by the Q-angle. Athletes, coaches, healthcare professionals, and athletic trainers can better comprehend and prepare for the benefits and drawbacks resulting from the Q-angle by familiarizing themselves with the research presented in this review.

Atrogin-1 and Muscle-specific RING finger protein 1 (MuRF1) are highly expressed in multiple conditions of skeletal muscle atrophy. The phosphoinositide 3-kinase (PI3K)/Akt/forkhead box (FoxO) signaling pathway is well known to regulate Atrogin-1 and MuRF1 gene expressions. However, Akt activation also activates the mechanistic target of rapamycin complex 1 (mTORC1), which induces skeletal muscle hypertrophy. Whether mTORC1-dependent signaling has a role in regulating Atrogin-1 and/or MuRF1 gene and protein expression is currently unclear. In this study, we showed that activation of insulin-mediated Akt signaling suppresses both Atrogin-1 and MuRF1 protein contents and that inhibition of Akt increases both Atrogin-1 and MuRF1 protein contents in C2C12 myotubes. Interestingly, inhibition of mTORC1 with a specific mTORC1 inhibitor, rapamycin, increased Atrogin-1, but not MuRF1, protein content. Furthermore, activation of AMP-activated protein kinase (AMPK), a negative regulator of the mTORC1 signaling pathway, also showed distinct time-dependent changes between Atrogin-1 and MuRF1 protein contents, suggesting differential regulatory mechanisms between Atrogin-1 and MuRF1 protein content. To further explore the downstream of mTORC1 signaling, we employed a specific S6K1 inhibitor, PF-4708671. We found that Atrogin-1 protein content was dose-dependently increased with PF-4708671 treatment, whereas MuRF1 protein content was decreased at 50 μM of PF-4708671 treatment. However, MuRF1 protein content was unexpectedly increased by PF-4708671 treatment for a longer period. Overall, our results indicate that Atrogin-1 and MuRF1 protein contents are regulated by different mechanisms, the downstream of Akt, and that Atrogin-1 protein content can be regulated by the rapamycin-sensitive mTOR-S6K1-dependent signaling pathway.

Muscle RING‐finger protein 1 (MuRF1, gene name: TRIM63 ) is well known as a critical molecular regulator in skeletal muscle atrophy. Despite the identification of several substrates and interaction partners for MuRF1, the precise molecular mechanisms by which MuRF1 causes skeletal muscle atrophy remain unclear. To gain further insight into the underlying mechanism of skeletal muscle atrophy, we applied targeted biochemical approaches and identified tripartite motif‐containing protein 72 (TRIM72) as a novel MuRF1‐interacting protein. Subsequent analysis using MuRF1 knockout and rescue experiments showed that TRIM72 protein abundance is dependent on the presence of MuRF1 protein. Furthermore, TRIM72 protein level was increased by dexamethasone treatment in C2C12 myotubes, alongside increased MuRF1 protein level. Dexamethasone decreases IRS1/Akt signaling and glucose uptake specifically in wild type myotubes, but not in MuRF1 KO myotubes. Further analysis showed that overexpression of TRIM72 impairs IRS1/Akt signaling without the presence of MuRF1, indicating that MuRF1 induces a negative impact on insulin signaling through a plausible cooperation with TRIM72. Our findings provide novel non‐degradative molecular roles of MuRF1 that link together skeletal muscle atrophy and impaired insulin sensitivity.

While exercise-induced haemorheological alterations are well-documented in various sports, the specific impact of a football match on red blood cell (RBC) parameters remains unknown. This study investigates the acute effects of a 90-minute football match on RBC indices in sedentary young males. After inclusion and exclusion criteria, twenty (20) moderately active, non-smoking male volunteers (mean age: 20.00 ± 0.4 years) participated in the study. Venous blood samples were collected pre- and post- football match to assess RBC count, haematocrit (HCT), and plasma volume (PV). Data generated were subjected to paired student's t-tests using SPSS, to compare values between pre- and post-match measurements. A p-value of less than 0.05 was considered indicative of statistical significance. The results showed a statistically significant decrease in haematocrit (HCT) and red blood cell count (RBC) after the match (p < 0.05) when compared to pre-match values. This was accompanied by a significant increase in plasma volume (PV) (p < 0.05), which was higher than pre-match values. These changes suggest that the physiological demands of the football match influenced blood parameters, likely due to fluid shifts and haemodilution during intense physical activity. These findings suggest potential implications for exercise physiology, diagnosis, and therapy in sports medicine.

Studies have revealed that athletes exhibit resting values of certain parameters that differ from those of the general population. This study aimed to assess the liver function status in football players and sedentary at rest. With a purposeful sampling technique, 20 male football players and 20 sedentary were recruited for this observational study following inclusion and exclusion criteria. The Ahmadu Bello University review board approved all procedures under the Declaration of Helsinki. Blood samples were taken at rest, to measure the liver function profiles. The independent t-test was used to compare the values. The level of significance was set at P< 0.05. Our result showed a significant decrease (p<0.05) in serum ALT activity (27.70 ± 2.1 IU/L vs 38.85 ± 3.0 IU/L) with a significant increase (p 0.05). These results suggested that regular football training increased liver function at rest. This observation has implications for sports medicine.