An examination of in-season external training load in semi-professional soccer players: considerations of one and two match weekly microcycles

The aim of the present study was to firstly, quantify the external training load (TL) of semi-professional soccer players during an annual season and secondly, to examine the influence of one (1MW) and two (2MW) match weekly microcycles. Data were collected from 24 semi-professional outfield soccer players during the 2018-2019 annual season using micro-electromechanical system (MEMS) devices for the following variables: Training duration (min), total distance (TD), Player Load (PL), high speed running (HSR) distance (5.5-7.0 m/s), and acceleration (ACC) efforts (>2 m/s2). Training sessions were defined as days before match day (i.e. MD minus), with match weeks broken down as either 1MW or 2MW. Data revealed higher TD, PL, and HSR distance on MD and MD-5 when compared to all other MD codes. MD-4 displayed significantly higher values compared to MD-1 (mean differences (Mdiff): TD: 785 ± 158 m; PL: 29 ± 9 au; HSR: 192 ± 63 m; ACC: 15 ± 3 #) and MD-2 (Mdiff: TD: 279 ± 137 m; HSR: 127 ± 54 m). During 2MW scenarios, both TD (Mdiff: 685 ± 328 m) and PL (Mdiff: 33 ± 14 au) were higher on MD-1 when compared to 1MW. However, lower values were observed for duration and HSR on MD-2 and MD-4 during 2MW compared to 1MW scenarios. These data suggest that there appears to be a progressive reduction in TD, PL, HSR and ACC leading into competitive matches based on MD- analysis. However, some variability exists in TL prescription as a result of different MW scenarios (i.e. 1MW vs. 2MW)

The HIF-PHI BAY 85–3934 (Molidustat) Improves Anemia and Is Associated With Reduced Levels of Circulating FGF23 in a CKD Mouse Model

Fibroblast growth factor-23 (FGF23) is a critical factor in chronic kidney disease (CKD), with elevated levels causing alterations in mineral metabolism and increased odds for mortality. Patients with CKD develop anemia as the kidneys progressively lose the ability to produce erythropoietin (EPO). Anemia is a potent driver of FGF23 secretion; therefore, a hypoxia-inducible factor prolyl hydroxylase inhibitor (HIF-PHI) currently in clinical trials to elevate endogenous EPO to resolve anemia was tested for effects on iron utilization and FGF23-related parameters in a CKD mouse model. Mice were fed either a casein control diet or an adenine-containing diet to induce CKD. The CKD mice had markedly elevated iFGF23 and blood urea nitrogen (BUN), hyperphosphatemia, and anemia. Cohorts of mice were then treated with a patient-equivalent dose of BAY 85-3934 (BAY; Molidustat), which elevated EPO and completely resolved aberrant complete blood counts (CBCs) in the CKD mice. iFGF23 was elevated in vehicle-treated CKD mice (120-fold), whereas circulating iFGF23 was significantly attenuated (>60%) in the BAY-treated CKD mice. The BAY-treated mice with CKD also had reduced BUN, but there was no effect on renal vitamin D metabolic enzyme expression. Consistent with increased EPO, bone marrow Erfe, Transferrin receptor (Tfrc), and EpoR mRNAs were increased in BAY-treated CKD mice, and in vitro hypoxic marrow cultures increased FGF23 with direct EPO treatment. Liver Bmp-6 and hepcidin expression were downregulated in all BAY-treated groups. Femur trabecular parameters and cortical porosity were not worsened with BAY administration. In vitro, differentiated osteocyte-like cells exposed to an iron chelator to simulate iron depletion/hypoxia increased FGF23; repletion with holo-transferrin completely suppressed FGF23 and normalized Tfrc1. Collectively, these results support that resolving anemia using a HIF-PHI during CKD was associated with lower BUN and reduced FGF23, potentially through direct restoration of iron utilization, thus providing modifiable outcomes beyond improving anemia for this patient population. © 2021 American Society for Bone and Mineral Research (ASBMR)

Somali Current rings in the eastern Gulf of Aden

Author Posting. © American Geophysical Union, 2006. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Journal of Geophysical Research 111 (2006): C09039, doi:10.1029/2005JC003338.New satellite-based observations reveal that westward translating anticyclonic rings are generated as a portion of the Somali Current accelerates northward through the Socotra Passage near the mouth of the Gulf of Aden. Rings thus formed exhibit azimuthal geostrophic velocities exceeding 50 cm/s, are comparable in overall diameter to the width of the Gulf of Aden (250 km), and translate westward into the gulf at 5–8 cm/s. Ring generation is most notable in satellite ocean color imagery in November immediately following the transition between southwest (boreal summer) and northeast (winter) monsoon regimes. The observed rings contain anomalous fluid within their core which reflects their origin in the equator-crossing Somali Current system. Estimates of Socotra Passage flow variability derived from satellite altimetry provide evidence for a similar ring generation process in May following the winter-to-summer monsoon transition. Cyclonic recirculation eddies are observed to spin up on the eastern flank of newly formed rings with the resulting vortex pair translating westward together. Recent shipboard and Lagrangian observations indicate that vortices of both sign have substantial vertical extent and may dominate the lateral circulation at all depths in the eastern Gulf of Aden.This investigation is a component of the Red Sea Outflow Experiment (REDSOX) sponsored by the U.S. National Science Foundation through grants OCE 98-18464 and OCE 04-24647 to the Woods Hole Oceanographic Institution and OCE 98-19506 and OCE 03-51116 to the University of Miami

Effect of clinical signs, endocrinopathies, timing of surgery, hyperlipidemia, and hyperbilirubinemia on outcome in dogs with gallbladder mucocele

Gallbladder mucocele (GBM) is a common extra-hepatic biliary syndrome in dogs with death rates ranging from 7 to 45%. Therefore, the aim of this study was to identify the association of survival with variables that could be utilized to improve clinical decisions. A total of 1194 dogs with a gross and histopathological diagnosis of GBM were included from 41 veterinary referral hospitals in this retrospective study. Dogs with GBM that demonstrated abnormal clinical signs had significantly greater odds of death than subclinical dogs in a univariable analysis (OR, 4.2; 95% CI, 2.14–8.23; P < 0.001). The multivariable model indicated that categorical variables including owner recognition of jaundice (OR, 2.12; 95% CI, 1.19–3.77; P = 0.011), concurrent hyperadrenocorticism (OR 1.94; 95% CI, 1.08–3.47; P = 0.026), and Pomeranian breed (OR, 2.46; 95% CI 1.10–5.50; P = 0.029) were associated with increased odds of death, and vomiting was associated with decreased odds of death (OR, 0.48; 95% CI, 0.30–0.72; P = 0.001). Continuous variables in the multivariable model, total serum/plasma bilirubin concentration (OR, 1.03; 95% CI, 1.01–1.04; P < 0.001) and age (OR, 1.17; 95% CI, 1.08–1.26; P < 0.001), were associated with increased odds of death. The clinical utility of total serum/plasma bilirubin concentration as a biomarker to predict death was poor with a sensitivity of 0.61 (95% CI, 0.54–0.69) and a specificity of 0.63 (95% CI, 0.59–0.66). This study identified several prognostic variables in dogs with GBM including total serum/plasma bilirubin concentration, age, clinical signs, concurrent hyperadrenocorticism, and the Pomeranian breed. The presence of hypothyroidism or diabetes mellitus did not impact outcome in this study.Supplemental Table S1. Number of dogs included from each institution and years reviewed.Supplemental Table S2. Included breeds.Supplemental Table S3. Distribution of various reasons given for performing cholecystectomy in the 179 subclinical dogs with gallbladder mucocele (GBM).Supplemental Table S4. Distribution of clinical signs associated with systemic illness in 982 dogs with gallbladder mucocele.Supplemental Table S5. Distribution of reasons for death in-hospital (i.e. euthanized and died) in 179 dogs with gallbladder mucocele that underwent cholecystectomy.http://www.elsevier.com/locate/tvjlhj2020Companion Animal Clinical Studie

Non-Testable Hypotheses in Linear Models

21 pages, 1 article*Non-Testable Hypotheses in Linear Models* (Searle, Shayle R.; Swallow, William H.; McCulloch, Charles E.) 21 page

Age and sex effects on FGF23-mediated response to mild phosphate challenge

Background: During aging, there is a normal and mild loss in kidney function that leads to abnormalities of the kidney-bone metabolic axis. In the setting of increased phosphorus intake, hyperphosphatemia can occur despite increased concentrations of the phosphaturic hormone FGF23. This is likely from decreased expression of the FGF23 co-receptor Klotho (KL) with age; however, the roles of age and sex in the homeostatic responses to mild phosphate challenges remain unclear. Methods: Male and female 16-week and 78-week mice were placed on either normal grain-based chow or casein (higher bioavailable phosphate) diets for 8 weeks. Gene expression, serum biochemistries, micro-computed tomography, and skeletal mechanics were used to assess the impact of mild phosphate challenge on multiple organ systems. Cell culture of differentiated osteoblast/osteocytes was used to test mechanisms driving key outcomes. Results: Aging female mice responded to phosphate challenge by significantly elevating serum intact FGF23 (iFGF23) versus control diet; males did not show this response. Male mice, regardless of age, exhibited higher kidney KL mRNA with similar phosphate levels across both sexes. However, males and females had similar blood phosphate, calcium, and creatinine levels irrespective of age, suggesting that female mice upregulated FGF23 to maintain blood phosphorus, and compromised renal function could not explain the increased serum iFGF23. The 17β-estradiol levels were not different between groups, and in vivo bone steroid receptor (estrogen receptor 1 [Esr1], estrogen receptor 2 [Esr2], androgen receptor [Ar]) expression was not different by age, sex, or diet. Trabecular bone volume was higher in males but decreased with both age and phosphate challenge in both sexes. Cortical porosity increased with age in males but not females. In vitro studies demonstrated that 17β-estradiol treatment upregulated FGF23 and Esr2 mRNAs in a dose-dependent manner. Conclusions: Our study demonstrates that aging female mice upregulate FGF23 to a greater degree during a mild phosphate challenge to maintain blood phosphorus versus young female and young/old male mice, potentially due to direct estradiol effects on osteocytes. Thus, the control of phosphate intake during aging could have modifiable outcomes for FGF23-related phenotypes

Time-course of muscle mass loss, Damage, and proteolysis in gastrocnemius following unloading and reloading: implications in chronic diseases.

BACKGROUND: Disuse muscle atrophy is a major comorbidity in patients with chronic diseases including cancer. We sought to explore the kinetics of molecular mechanisms shown to be involved in muscle mass loss throughout time in a mouse model of disuse muscle atrophy and recovery following immobilization. METHODS: Body and muscle weights, grip strength, muscle phenotype (fiber type composition and morphometry and muscle structural alterations), proteolysis, contractile proteins, systemic troponin I, and mitochondrial content were assessed in gastrocnemius of mice exposed to periods (1, 2, 3, 7, 15 and 30 days) of non-invasive hindlimb immobilization (plastic splint, I cohorts) and in those exposed to reloading for different time-points (1, 3, 7, 15, and 30 days, R cohorts) following a seven-day period of immobilization. Groups of control animals were also used. RESULTS: Compared to non-exposed controls, muscle weight, limb strength, slow- and fast-twitch cross-sectional areas, mtDNA/nDNA, and myosin content were decreased in mice of I cohorts, whereas tyrosine release, ubiquitin-proteasome activity, muscle injury and systemic troponin I levels were increased. Gastrocnemius reloading following splint removal improved muscle mass loss, strength, fiber atrophy, injury, myosin content, and mtDNA/nDNA, while reducing ubiquitin-proteasome activity and proteolysis. CONCLUSIONS: A consistent program of molecular and cellular events leading to reduced gastrocnemius muscle mass and mitochondrial content and reduced strength, enhanced proteolysis, and injury, was seen in this non-invasive mouse model of disuse muscle atrophy. Unloading of the muscle following removal of the splint significantly improved the alterations seen during unloading, characterized by a specific kinetic profile of molecular events involved in muscle regeneration. These findings have implications in patients with chronic diseases including cancer in whom physical activity may be severely compromised.This study has been supported by the following Spanish agencies: CIBERES, PI14/00713 (FEDER), and SAF-2014-54371-R (FEDER) from the Instituto de Salud Carlos III (http://www.isciii.es/); SEPAR 2013 and SEPAR 2016 from Spanish Respiratory Society (SEPAR, http://www.separ.es/); and Catalan Foundation of Pneumology (FUCAP, http://www.ccfundacions.cat/fundacions/fundacio-catalana-de-pneumologia-fucap), FUCAP 201