Relationship between the strength of the hip and knee stabilizer muscles and the Y balance test performance in adolescent volleyball athletes.

BACKGROUND: Due to the large number of jumping and landing movements, volleyball exerts a high demand on lower limbs, causing a high incidence of injuries. On average, 52% of volleyball injuries occur in lower limbs. Y Balance-test (YBT) is widely used to predict lower limb injury in athletes who jump, so it is important to identify whether the hip and knee stabilizer muscle strength is related to the performance of this test, since muscle strength is important for injury prevention, given the possibility of modifying these factors. The aim of this cross-sectional study was to correlate the strength of the knee and hip stabilizing muscles with YBT in adolescent volleyball athletes. METHODS: A study including 25 young volleyball players (aged 15.3 [0.85] years), was evaluated. The isometric strength of knee extensor muscles, abductors, extensors and lateral hip rotators were assessed by using the manual isometric dynamometer (Lafaytte Instrument Company®, Lafayette, IN, USA). YBT was performed three times on each posterolateral (PL), anterior (ANT) and posteromedial (PM) direction to evaluate the dominant leg. The average of 3 repetitions of isometric strength tests of tested muscles and YBT was analyzed. Pearson's Correlation test was used for the correlation of the variables, considering as strong correlation values (0.5≤r<1), with P≤0.05. RESULTS: A moderate correlation was observed between the knee extensor strength and the ANT direction, and a moderate correlation between the hip extensor strength and the PL direction in YBT. CONCLUSIONS: The strength of knee and hip extensors may be one of the factors that influence the performance of YBT in adolescent volleyball players.

The effect of BPA exposure on insulin resistance and type 2 diabetes - The impact of muscle contraction.

Type 2 diabetes (T2D) is considered one of the leading causes of death worldwide. In addition to physical inactivity and obesity, established risk factors for T2D, chemical contaminants consumed in industrialized food such as BPA might also be a contributor to the development of T2D. Epidemiological studies have shown that BPA concentrations are higher in human specimens of T2D when compared to healthy subjects, while experimental studies suggested that bisphenol A (BPA) impairs the pathway by which insulin stimulates glucose uptake. In skeletal muscle and adipocytes, insulin resistance is developed by the impairment of the insulin pathway to stimulate the translocation of glucose transporter, GLUT4, to the cell membrane. Recent results demonstrated that BPA impairs several components of insulin-induced glucose uptake pathway and affect the expression of GLUT4. Regular physical exercise delays or inhibits the development of T2D due to the physiologic processes taking place during muscle contraction, and the fact that skeletal muscle is the site for almost 80% of the glucose transported under insulin stimulation. In fact, the mechanism by which contraction induces glucose uptake in skeletal muscle is partially independent of the insulin pathway, therefore, the effect of BPA on this mechanism is unknown. We hypothesize that during the development of insulin resistance, BPA contributes to the impairment of the molecular pathway by which insulin induces glucose uptake while contraction-induced glucose uptake is not impaired. At the late stages of T2D, BPA may affect GLUT4 expression that will decrease the ability of muscle contraction to induce glucose uptake.

Abrogation of MMP-9 gene protects against the development of retinopathy in diabetic mice by preventing mitochondrial damage.

OBJECTIVE: In the development of diabetic retinopathy, mitochondrial dysfunction is considered to play an important role in the apoptosis of retinal capillary cells. Diabetes activates matrix metalloproteinase-9 (MMP-9) in the retina and its capillary cells, and activated MMP-9 becomes proapoptotic. The objective of this study is to elucidate the plausible mechanism by which active MMP-9 contributes to the mitochondrial dysfunction in the retina. RESEARCH DESIGN AND METHODS: Using MMP-9 gene knockout (MMP-KO) mice, we investigated the effect of MMP-9 regulation on diabetes-induced increased retinal capillary cell apoptosis, development of retinopathy, mitochondrial dysfunction and ultrastructure, and mitochondrial DNA (mtDNA) damage. To understand how diabetes increases mitochondrial accumulation of MMP-9, interactions between MMP-9 and chaperone proteins (heat shock protein [Hsp] 70 and Hsp60) were evaluated. The results were confirmed in the retinal mitochondria from human donors with diabetic retinopathy, and in isolated retinal endothelial cells transfected with MMP-9 small interfering RNA (siRNA). RESULTS: Retinal microvasculature of MMP-KO mice, diabetic for ∼7 months, did not show increased apoptosis and pathology characteristic of retinopathy. In the same MMP-KO diabetic mice, activation of MMP-9 and dysfunction of the mitochondria were prevented, and electron microscopy of the retinal microvasculature region revealed normal mitochondrial matrix and packed lamellar cristae. Damage to mtDNA was protected, and the binding of MMP-9 with Hsp70 or Hsp60 was also normal. As in the retina from wild-type diabetic mice, activation of mitochondrial MMP-9 and alterations in the binding of MMP-9 with chaperone proteins were also observed in the retina from donors with diabetic retinopathy. In endothelial cells transfected with MMP-9 siRNA, high glucose-induced damage to the mitochondria and the chaperone machinery was ameliorated. CONCLUSIONS: Regulation of activated MMP-9 prevents retinal capillary cells from undergoing apoptosis by protecting mitochondrial ultrastructure and function and preventing mtDNA damage. Thus, MMP-9 inhibitors could have potential therapeutic value in preventing the development of diabetic retinopathy by preventing the continuation of the vicious cycle of mitochondrial damage.