Influence of dynamic stretching on ankle joint stiffness, vertical stiffness and running economy during treadmill running

Data availability statement: The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.Copyright © 2022 Pamboris, Noorkoiv, Baltzopoulos, Powell, Howes and Mohagheghi. The purpose of the present study was to investigate whether and how dynamic stretching of the plantarflexors may influence running economy. A crossover design with a minimum of 48 h between experimental (dynamic stretching) and control conditions was used. Twelve recreational runners performed a step-wise incremental protocol to the limit of tolerance on a motorised instrumented treadmill. The initial speed was 2.3 m/s, followed by increments of 0.2 m/s every 3 min. Dynamic joint stiffness, vertical stiffness and running kinematics during the initial stage of the protocol were calculated. Running economy was evaluated using online gas-analysis. For each participant, the minimum number of stages completed before peak O2 uptake (V̇O2peak) common to the two testing conditions was used to calculate the gradient of a linear regression line between V̇O2 (y-axis) and speed (x-axis). The number of stages, which ranged between 4 and 8, was used to construct individual subject regression equations. Non-clinical forms of magnitude-based decision method were used to assess outcomes. The dynamic stretching protocol resulted in a possible decrease in dynamic ankle joint stiffness (−10.7%; 90% confidence limits ±16.1%), a possible decrease in vertical stiffness (−2.3%, ±4.3%), a possibly beneficial effect on running economy (−4.0%, ±8.3%), and very likely decrease in gastrocnemius medialis muscle activation (−27.1%, ±39.2%). The results indicate that dynamic stretching improves running economy, possibly via decreases in dynamic joint and vertical stiffness and muscle activation. Together, these results imply that dynamic stretching should be recommended as part of the warm-up for running training in recreational athletes examined in this study

Influence of dynamic stretching on ankle joint stiffness, vertical stiffness and running economy during treadmill running

The purpose of the present study was to investigate whether and how dynamic stretching of the plantarflexors may influence running economy. A crossover design with a minimum of 48 h between experimental (dynamic stretching) and control conditions was used. Twelve recreational runners performed a step-wise incremental protocol to the limit of tolerance on a motorised instrumented treadmill. The initial speed was 2.3 m/s, followed by increments of 0.2 m/s every 3 min. Dynamic joint stiffness, vertical stiffness and running kinematics during the initial stage of the protocol were calculated. Running economy was evaluated using online gas-analysis. For each participant, the minimum number of stages completed before peak O2 uptake (V̇O2peak) common to the two testing conditions was used to calculate the gradient of a linear regression line between V̇O2 (y-axis) and speed (x-axis). The number of stages, which ranged between 4 and 8, was used to construct individual subject regression equations. Non-clinical forms of magnitude-based decision method were used to assess outcomes. The dynamic stretching protocol resulted in a possible decrease in dynamic ankle joint stiffness (−10.7%; 90% confidence limits ±16.1%), a possible decrease in vertical stiffness (−2.3%, ±4.3%), a possibly beneficial effect on running economy (−4.0%, ±8.3%), and very likely decrease in gastrocnemius medialis muscle activation (−27.1%, ±39.2%). The results indicate that dynamic stretching improves running economy, possibly via decreases in dynamic joint and vertical stiffness and muscle activation. Together, these results imply that dynamic stretching should be recommended as part of the warm-up for running training in recreational athletes examined in this study

A knowledge translation collaborative to improve the use of therapeutic hypothermia in post-cardiac arrest patients: protocol for a stepped wedge randomized trial

<p>Abstract</p> <p>Background</p> <p>Advances in resuscitation science have dramatically improved survival rates following cardiac arrest. However, about 60% of adults that regain spontaneous circulation die before leaving the hospital. Recently it has been shown that inducing hypothermia in cardiac arrest survivors immediately following their arrival in hospital can dramatically improve both overall survival and neurological outcomes. Despite the strong evidence for its efficacy and the apparent simplicity of this intervention, recent surveys show that therapeutic hypothermia is delivered inconsistently, incompletely, and often with delay.</p> <p>Methods and design</p> <p>This study will evaluate a multi-faceted knowledge translation strategy designed to increase the utilization rate of induced hypothermia in survivors of cardiac arrest across a network of 37 hospitals in Southwestern Ontario, Canada. The study is designed as a stepped wedge randomized trial lasting two years. Individual hospitals will be randomly assigned to four different wedges that will receive the active knowledge translation strategy according to a sequential rollout over a number of time periods. By the end of the study, all hospitals will have received the intervention. The primary aim is to measure the effectiveness of a multifaceted knowledge translation plan involving education, reminders, and audit-feedback for improving the use of induced hypothermia in survivors of cardiac arrest presenting to the emergency department. The primary outcome is the proportion of eligible OHCA patients that are cooled to a body temperature of 32 to 34°C within six hours of arrival in the hospital. Secondary outcomes will include process of care measures and clinical outcomes.</p> <p>Discussion</p> <p>Inducing hypothermia in cardiac arrest survivors immediately following their arrival to hospital has been shown to dramatically improve both overall survival and neurological outcomes. However, this lifesaving treatment is frequently not applied in practice. If this trial is positive, our results will have broad implications by showing that a knowledge translation strategy shared across a collaborative network of hospitals can increase the number of patients that receive this lifesaving intervention in a timely manner.</p> <p>Trial Registration</p> <p>ClinicalTrials.gov Trial Identifier: <a href="http://www.clinicaltrials.gov/ct2/show/NCT00683683">NCT00683683</a></p

Schizophrenia: do all roads lead to dopamine or is this where they start? Evidence from two epidemiologically informed developmental rodent models

The idea that there is some sort of abnormality in dopamine (DA) signalling is one of the more enduring hypotheses in schizophrenia research. Opinion leaders have published recent perspectives on the aetiology of this disorder with provocative titles such as ‘Risk factors for schizophrenia—all roads lead to dopamine' or ‘The dopamine hypothesis of schizophrenia—the final common pathway'. Perhaps, the other most enduring idea about schizophrenia is that it is a neurodevelopmental disorder. Those of us that model schizophrenia developmental risk-factor epidemiology in animals in an attempt to understand how this may translate to abnormal brain function have consistently shown that as adults these animals display behavioural, cognitive and pharmacological abnormalities consistent with aberrant DA signalling. The burning question remains how can in utero exposure to specific (environmental) insults induce persistent abnormalities in DA signalling in the adult? In this review, we summarize convergent evidence from two well-described developmental animal models, namely maternal immune activation and developmental vitamin D deficiency that begin to address this question. The adult offspring resulting from these two models consistently reveal locomotor abnormalities in response to DA-releasing or -blocking drugs. Additionally, as adults these animals have DA-related attentional and/or sensorimotor gating deficits. These findings are consistent with many other developmental animal models. However, the authors of this perspective have recently refocused their attention on very early aspects of DA ontogeny and describe reductions in genes that induce or specify dopaminergic phenotype in the embryonic brain and early changes in DA turnover suggesting that the origins of these behavioural abnormalities in adults may be traced to early alterations in DA ontogeny. Whether the convergent findings from these two models can be extended to other developmental animal models for this disease is at present unknown as such early brain alterations are rarely examined. Although it is premature to conclude that such mechanisms could be operating in other developmental animal models for schizophrenia, our convergent data have led us to propose that rather than all roads leading to DA, perhaps, this may be where they start

A short history of the 5-HT2C receptor: from the choroid plexus to depression, obesity and addiction treatment

This paper is a personal account on the discovery and characterization of the 5-HT2C receptor (first known as the 5- HT1C receptor) over 30 years ago and how it translated into a number of unsuspected features for a G protein-coupled receptor (GPCR) and a diversity of clinical applications. The 5-HT2C receptor is one of the most intriguing members of the GPCR superfamily. Initially referred to as 5-HT1CR, the 5-HT2CR was discovered while studying the pharmacological features and the distribution of [3H]mesulergine-labelled sites, primarily in the brain using radioligand binding and slice autoradiography. Mesulergine (SDZ CU-085), was, at the time, best defined as a ligand with serotonergic and dopaminergic properties. Autoradiographic studies showed remarkably strong [3H]mesulergine-labelling to the rat choroid plexus. [3H]mesulergine-labelled sites had pharmacological properties different from, at the time, known or purported 5-HT receptors. In spite of similarities with 5-HT2 binding, the new binding site was called 5-HT1C because of its very high affinity for 5-HT itself. Within the following 10 years, the 5-HT1CR (later named 5- HT2C) was extensively characterised pharmacologically, anatomically and functionally: it was one of the first 5-HT receptors to be sequenced and cloned. The 5-HT2CR is a GPCR, with a very complex gene structure. It constitutes a rarity in theGPCR family: many 5-HT2CR variants exist, especially in humans, due to RNA editing, in addition to a few 5-HT2CR splice variants. Intense research led to therapeutically active 5-HT2C receptor ligands, both antagonists (or inverse agonists) and agonists: keeping in mind that a number of antidepressants and antipsychotics are 5- HT2CR antagonists/inverse agonists. Agomelatine, a 5-HT2CR antagonist is registered for the treatment of major depression. The agonist Lorcaserin is registered for the treatment of aspects of obesity and has further potential in addiction, especially nicotine/ smoking. There is good evidence that the 5-HT2CR is involved in spinal cord injury-induced spasms of the lower limbs, which can be treated with 5-HT2CR antagonists/inverse agonists such as cyproheptadine or SB206553. The 5-HT2CR may play a role in schizophrenia and epilepsy. Vabicaserin, a 5-HT2CR agonist has been in development for the treatment of schizophrenia and obesity, but was stopped. As is common, there is potential for further indications for 5-HT2CR ligands, as suggested by a number of preclinical and/or genome-wide association studies (GWAS) on depression, suicide, sexual dysfunction, addictions and obesity. The 5-HT2CR is clearly affected by a number of established antidepressants/antipsychotics and may be one of the culprits in antipsychotic-induced weight gain

The Role of SPRASA in Female Fertility

Fertility is a complex process and infertility can have many causes. Sperm protein reactive with antisperm antibody (SPRASA)/sperm lysozyme-like protein 1 is a protein discovered as the target of autoantibodies in infertile men and previously thought to be expressed only in sperm. Using a bovine in vitro fertilization model, we have shown that SPRASA antiserum reduced sperm binding to zona-free oocytes and the development of embryos to morulae but did not affect the postfertilization cleavage rate to 2 cells or sperm motility. We demonstrated that SPRASA was expressed in ovarian follicles, corpora lutea, and oocytes by a combination of reverse transcription-polymerase chain reaction and immunohistochemistry. Female mice immunized with SPRASA had profound infertility following timed matings and those mice that did become pregnant had reduced fetal viability. The levels of antibodies reactive with SPRASA in 204 fertile and 202 infertile couples were elevated in 3 infertile but no fertile women. Together, these results indicate that SPRASA has a role in female fertility.Full Tex