Physiology international最新文献

In this study, the ability of microRNA-1906 (miR-1906) to attenuate bone loss in osteoporosis was evaluated by measuring the effects of a miR-1906 mimic and inhibitor on the cellular toxicity and cell viability of MC3T3-E1 cells. Bone marrow-derived macrophage (BMM) cells were isolated from female mice, and tartrate-resistant acid phosphatase signalling was performed in miR-1906 mimic-treated, receptor-activated nuclear factor kappa-B (NF-κB) ligand (RANKL)-induced osteoclasts. In-vivo, osteoporosis was induced by ovariectomy (OVX). Rats were treated with 500 nmol/kg of the miR-1906 mimic via intrathecal administration for 10 consecutive days following surgery. The effect of the miR-1906 mimic on bone mineral density (BMD) in OVX rats was observed in the whole body, lumbar vertebrae and femur. Levels of biochemical parameters and cytokines in the serum of miR-1906 mimic-treated OVX rats were analysed. The mRNA expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), p-38 and NF-κB in tibias of osteoporotic rats (induced by ovariectomy) was observed using quantitative reverse-transcription polymerase chain reaction. Treatment with the miR-1906 mimic reduced cellular toxicity and enhanced the cell viability of MC3T3-E1 cells. Furthermore, osteoclastogenesis in miR-1906 mimic-treated, RANKL-induced osteoclast cells was reduced, whereas the BMD in the miR-1906 mimic-treated group was higher than in the OVX group of rats. Treatment with the miR-1906 mimic also increased levels of biochemical parameters and cytokines in the serum of ovariectomised rats. Finally, mRNA expression levels of TLR4, MyD88, p-38 and NF-κB were lower in the tibias of miR-1906 mimic-treated rats than in those of OVX rats. In conclusion, the miR-1906 mimic reduces bone loss in rats with ovariectomy-induced osteoporosis by regulating the TLR4/MyD88/NF-κB pathway.

Objective: The aim of the present study was to analyse the relationships between creatine kinase (CK) concentration, an indirect marker of muscle damage, and global positioning system (GPS)-derived metrics of a continuous two-week-long preseason training period in elite football.

Design: Twenty-one elite male professional soccer players were assessed during a 14-day preseason preparatory period. CK concentrations were determined each morning, and a GPS system was used to quantify the external load. A generalized estimating equation (GEE) model was established to determine the extent to which the external load parameter explained post-training CK levels.

Results: The GEE model found that higher numbers of decelerations (χ 2 = 7.83, P = 0.005) were most strongly associated with the post-training CK level. Decelerations and accelerations accounted for 62% and 11% of the post-training CK level, respectively, and considerable interindividual variability existed in the data.

Conclusion: The use of GPS to predict muscle damage could be of use to coaches and practitioners in prescribing recovery practices. Based on GPS data, more individualized strategies could be devised and could potentially result in better subsequent performance.

Aim: Limited investigations on metabolic responses to exercise training in female adolescent volleyball athletes exist. The aim of this study was to obtain serum and urine metabolite markers in female adolescent volleyball athletes within 2-week strength-endurance training using a metabolomics approach coupled with biochemical analysis, which would be potential biomarkers for evaluating the physiological state of athletes.

Methods: Twelve female adolescent volleyball athletes were recruited for 2-week strength-endurance training. Differential serum and urine metabolic profiles between the pre- and post-training group were obtained on gas chromatography coupled to mass spectrometry (GC-MS) and data subsequently underwent orthogonal partial least-squares analysis (OPLS).

Results: Strength-endurance training exerted a significant influence on the athletes' serum and urine metabolic profiles. The changed metabolites were primarily involved in energy metabolism, lipid metabolism and amino acids metabolism. Results support the hypothesis that female athletes displayed an increased propensity to oxidize lipids as the major energy source. Exposure to strength-endurance training also led to a significant increase in cortisol, but a decrease in testosterone, indicating disordered hormone adjustment. Exercise-induced oxidative stress occurred, as was evidenced by the decrease in reduced glutathione, and increases in blood malondialdehyde and oxidized glutathione. Since the muscle damage markers creatine kinase and lactate dehydrogenase did not show significant changes, the training might not cause cell membrane damage and the athletes did not cross the adaptive injury level.

Conclusion: By measurement of endogenous metabolites, the metabolomics study has the potential to reveal the global physiological changes in response to exercise training.

Based on the current literature, the link between Achilles tendon moment arm length and running economy is not well understood. Therefore, the aim of this study was to further investigate the connection between Achilles tendon moment arm and running economy and the influence of Achilles tendon moment arm on the function of the plantarflexor muscle-tendon unit during running.Ten male competitive marathon runners volunteered for this study. The participants ran on a treadmill at two running speeds: 3 and 3.5 m s-1. During running the oxygen consumption, lower leg kinematics, electrical activity of plantar flexor muscles, and fascicle behavior of the lateral gastrocnemius were measured simultaneously. On the second occasion, an MRI scan of the right leg was taken and used to estimate the Achilles tendon moment arm length.There was a negative correlation between running economy and the body height normalized moment arm length at both selected speeds (r = -0.68, P = 0.014 and r = -0.70, P = 0.01). In addition, Achilles tendon moment arm length correlated with the amplitude of the ankle flexion at both speeds (r = -0.59, P = 0.03 and r = -0.60, P = 0.03) and with the electrical activity of the medial gastrocnemius muscle at 3 m s-1 speed (r = -0.62, P = 0.02). Our finding supports the concept that a longer moment arm could be beneficial for distance runners.

Introduction: Increased oxidative/nitrative stress is characteristic not only in pathologic, but also in healthy pregnancy. High uterine artery pulsatility index (UtAPI) at the end of the first trimester is associated with altered placentation and elevated risk for adverse pregnancy outcomes. We aimed to examine the relationship of systemic oxidative/nitrative stress and uterine artery pulsatility index in the first trimester and their correlation to pregnancy outcomes.

Material and methods: Healthy pregnant women were recruited at 12-13th gestational week ultrasound examination; UtAPI was determined by color Doppler ultrasound. Patients were divided into high (UtAPI ≥ 2.3) (n = 30) and low (n = 31) resistance groups, and pregnancies were followed until labor. Systemic oxidative/nitrative stress was estimated by measuring total peroxide level, total antioxidant capacity and nitrotyrosine level.

Results: Plasma total peroxide level was significantly lower (2,510 ± 39 µM vs. 2,285 ± 59 µM), total antioxidant capacity was higher (781 ± 16 mM CRE vs. 822 ± 13 mM CRE) in the high UtAPI group, which were accompanied by lower birth weight (3,317 ± 64 vs. 3,517 ± 77 g, P < 0.05). Plasma total peroxide level showed a negative correlation (by Pearson) to UtAPI (P < 0.01) and positive correlation to birth weight (P < 0.05).

Conclusions: According to our results, lower systemic oxidative stress showed correlation with high UtAPI measured between the 12-13th weeks of gestation. We also found significant differences in the birth weight of healthy newborns; therefore it is worth examining this relationship in pathological pregnancies.

Irisin is a novel exercise-induced myokine that may be involved in regulating energy metabolism. We determined whether overtraining syndrome (OTS) and its biochemical markers are associated with plasma irisin levels in athletes. Seven severely overtrained athletes (OA) and 10 healthy control athletes (CA) were recruited and examined at the time of diagnosis (baseline) and after 6- and 12-months follow-up. Training volume and intensity were initially restricted but progressively increased in OA as OTS symptoms alleviated; CA continued their normal training routine. A maximal cycle ergometer test was performed with irisin analyzed before and after the test. Before the exercise test, irisin levels tended to be lower in OA than in CA at baseline (154.5 ± 28.5 vs. 171.7 ± 58.7 ng/mL). In both groups, at rest irisin levels changed only marginally during follow-up and were not affected by maximal exercise, nor were they associated with physical performance or body fat percentage. Irisin concentration at rest correlated positively with an oxidative stress marker, malondialdehyde (MDA) and negatively with an antioxidant protection marker, oxygen radical absorbance capacity (ORAC) in response to the exercise test in OA at baseline. Our findings help to clarify the possible contribution of irisin and its association with oxidative stress in the pathophysiology of OTS.

We aimed to analyse the complexity and fractal nature of heartbeat during constant exercise, at three different intensities, and recovery.Fourteen healthy men underwent 4 separate sessions. The first session was an incremental treadmill test to determine ventilatory thresholds (VT1 and VT2) and maximal aerobic speed (MAS). Each subject ran at VT1 and VT2 speeds and MAS (second, third and fourth day). The duration of VT1 and VT2 loads were selected in such a way that the product intensity-duration (training load) was the same. Sample Entropy (SampEn) and slope of Detrended Fluctuation Analysis (DFA α1) were measured during the whole session.DFA α1 declines with exercise, being less in the VT1 trial than in the other two.SampEn shows no significant change during exercise. The three tests induce the same decline in SampEn, but at the highest intensity (MAS) tends to decline during the exercise itself, whereas at lower intensities (VT1, VT2) the decline is delayed (10 min of recovery). Subsequently, SampEn at VT1 gradually recovers, whereas at VT2 and MAS it remains stable during recovery.In conclusion, exercise produces a loss of heartbeat complexity, but not fractal nature, during recovery and it depends on intensity.

An imbalance between calorie intake and energy expenditure produces obesity. It has been a major problem in societies of the developing and developed world. In obesity an excessive amount of fat accumulates in adipose tissue cells as well as in other vital organs like liver, muscles, and pancreas. The adipocytes contain ob genes and express leptin, a 16 kDa protein. In the present communication, we reviewed the molecular basis of the etiopathophysiology of leptin in obesity. Special emphasis has been given to the use of leptin as a drug target for obesity treatment, the role of diet in the modulation of leptin secretion, and reduction of obesity at diminished level of blood leptin induced by physical exercise.

Background: To investigate the serum level of hepcidin and its relationship with cardiovascular disease (CVD) in maintenance hemodialysis (MHD) patients.

Methods: Blood was obtained from 75 MHD patients before undergoing hemodialysis and 20 healthy controls. Serum hepcidin, advanced oxidation protein products (AOPP) and interleukin (IL)-6 were measured by enzyme-linked immunosorbant assay (ELISA). Spearman correlation, and binary logistic regression linear regression analyses were used to assess the relationship between serum hepcidin and other parameters.

Results: The serum level of hepcidin, AOPP and IL-6 was significantly up-regulated in MHD patients compared with the control (P < 0.05). Furthermore, serum hepcidin levels in patients with CVD were higher than those in patients without CVD (P < 0.05). In all MHD patients, serum hepcidin level was correlated positively with erythropoietin (EPO) dose per week (ρ = 0.251, P = 0.030), EPO resistance index (ρ = 0.268, P = 0.020), ferritin (ρ = 0.814, P < 0.001), transferin saturation (TSAT, ρ = 0.263, P = 0.023), AOPP (ρ = 0.280, P = 0.049), high sensitive C reactive protein (ρ = 0.151, P = 0.006), IL-6 (ρ = 0.340, P = 0.003) and left ventricular mass index (LVMI, ρ = 0.290, P = 0.033). Moreover, it was negatively correlated with serum pre-albumin (ρ = -0.266, P = 0.021), total iron-binding capacity (TIBC, ρ = -0.458, P < 0.001), unsaturated iron-binding capacity (UIBC, ρ = -0.473, P < 0.001) and transferrin (ρ = -0.487, P < 0.001). Linear regression analysis showed that ferritin (β = 0.708, P < 0.001), TIBC (β = -0.246, P = 0.032) and IL-6 (β = 0.209, P = 0.041) were independently associated with hepcidin. Results of binary logistic regression analysis suggested that higher serum hepcidin level (>249.2 ng/mL) was positively and independently related to CVD (OR = 1.32, 95% CI [1.20-9.56], P = 0.043).

Conclusions: Serum hepcidin level is associated with CVD in MHD patients, indicating that hepcidin may be a novel biomarker and therapeutic target for CVD.

Purpose: Progesterone has been reported to inhibit the proliferation of breast cancer and osteosarcoma cells; however, its inhibitory mechanism has not yet been clarified. The aim of the present study was to clarify the effects of progesterone on apoptosis in breast cancer (MCF-7) and human osteosarcoma (MG-63) cells.

Materials and methods: In this experimental study the cytotoxic effect of progesterone was measured in MCF-7 and MG-63 cells exposed to different concentrations of progesterone using MTT assay, and effective concentrations were identified. The expression levels of the Bax, P53 and Bcl-2 genes were evaluated by real-time PCR, and caspase-3, 8 and 9 activity levels were determined using a colorimetric method. Hoechst staining and flow cytometry were used to confirm apoptosis. The data were statistically analyzed using one-way analysis of variance (ANOVA) and independent-samples t-test.

Results: Compared to the control group, we observed a significant increase in the expression levels of the Bax and P53 genes and the activity levels of caspase-3 and 9, and a significant decrease in the expression level of the Bcl-2 gene in MCF-7 and MG-63 treated with effective concentration of progesterone. The caspase-8 activity level did not change significantly in treated MG-63 but increased in treated MCF-7 cells. Hoechst staining and flow cytometry results confirmed apoptosis in the cells exposed to effective concentration of progesterone.

Conclusions: The cytotoxic effect of progesterone on breast cancer and osteosarcoma cells was mediated by apoptotic pathways. In this context, progesterone triggers the extrinsic and intrinsic apoptotic pathways in MCF-7 cells and induces the intrinsic apoptotic pathway in MG-63 cells.