41 research outputs found

    Kinematic variations due to changes in pace during men's and women's 5 km road running

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    The purpose of this study was to investigate variations in kinematic parameters in men's and women's 5 km road racing. Athletes often vary their pace and changes particularly tend to occur towards the end of a race due to fatigue and sprint finishes. Twenty competitive distance runners (10 male, 10 female) were videoed as they completed the English National 5 km championships. Three-dimensional kinematic data were analysed using motion analysis software (SIMI, Munich). Data were recorded at 950 m, 2,400 m and 3,850 m. Repeated measures ANOVA showed significant decreases in speed due to reduced step length and cadence in both men and women. These decreases predominantly occurred between the first two measurement points. The hip, knee, ankle and shoulder angles at both initial contact and toe-off did not change significantly, but there were significant reductions in the elbow angle for both men (at initial contact) and women (at toe-off)

    Alzheimer's Amyloid-β is an Antimicrobial Peptide: A Review of the Evidence

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    The final publication is available at IOS Press through http://dx.doi.org/10.3233/JAD-171133.The amyloid-β (Aβ) peptide has long been considered to be the driving force behind Alzheimer’s disease (AD). However, clinical trials that have successfully reduced Aβ burden in the brain have not slowed the cognitive decline, and in some instances, have resulted in adverse outcomes. While these results can be interpreted in different ways, a more nuanced picture of Aβ is emerging that takes into account the facts that the peptide is evolutionarily conserved and is present throughout life in cognitively normal individuals. Recent evidence indicates a role for Aβ as an antimicrobial peptide (AMP), a class of innate immune defense molecule that utilizes fibrillation to protect the host from a wide range of infectious agents. In humans and in animal models, infection of the brain frequently leads to increased amyloidogenic processing of the amyloid-β protein precursor (AβPP) and resultant fibrillary aggregates of Aβ. Evidence from in vitro and in vivo studies demonstrates that Aβ oligomers have potent, broad-spectrum antimicrobial properties by forming fibrils that entrap pathogens and disrupt cell membranes. Importantly, overexpression of Aβ confers increased resistance to infection from both bacteria and viruses. The antimicrobial role of Aβ may explain why increased rates of infection have been observed in some of the AD clinical trials that depleted Aβ. Perhaps progress toward a cure for AD will accelerate once treatment strategies begin to take into account the likely physiological functions of this enigmatic peptide.The Ohio State UniversityManuscript post-prin

    Effects of deceptive running speed on physiology, perceptual responses, and performance during sprint-distance triathlon

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    Objective This study examined the effects of speed deception on performance, physiological and perceptual responses, and pacing during sprint-distance triathlon running. Methods Eight competitive triathletes completed three simulated sprint-distance triathlons (0.75 km swim, 20 km bike, 5 km run) in a randomised order, with swimming and cycling sections replicating baseline triathlon performance. During the first 1.66 km of the run participants maintained an imposed speed, completing the remaining 3.33 km as quickly as possible. Although participants were informed that initially prescribed running speed would reflect baseline performance, this was true during only one trial (Tri-Run100%). As such, other trials were either 3% faster (Tri-Run103%), or 3% slower (Tri-Run97%) than baseline during this initial period. Results Performance during Tri-Run103% (1346 ± 108 s) was likely faster than Tri-Run97% (1371 ± 108 s), and possibly faster than Tri-Run100% (1360 ± 125 s), with these differences likely to be competitively meaningful. The first 1.66 km of Tri-Run103% induced greater physiological strain compared to other conditions, whilst perceptual responses were not significantly different between trials. Conclusions It appears that even during ‘all-out’ triathlon running, athletes maintain some form of ‘reserve’ capacity which can be accessed by deception. This suggests that expectations and beliefs have a practically meaningful effect on pacing and performance during triathlon, although it is apparent that an individual’s conscious intentions are secondary to the brains sensitivity to potentially harmful levels of physiological and perceptual strain

    Deceptive Manipulation of Competitive Starting Strategies Influences Subsequent Pacing, Physiological Status, and Perceptual Responses during Cycling Time Trials

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    The provision of performance-related feedback during exercise is acknowledged as an influential external cue used to inform pacing decisions. The provision of this feedback in a challenging or deceptive context allows research to explore how feedback can be used to improve performance and influence perceptual responses. However, the effects of deception on both acute and residual responses have yet to be explored, despite potential application for performance enhancement. Therefore, this study investigated the effects of challenging and deceptive feedback on perceptual responses and performance in self-paced cycling time trials (TT) and explored whether changes in performance are sustained in a subsequent TT following the disclosure of the deception. Seventeen trained male cyclists were assigned to either an accurate or deceptive feedback group and performed four 16.1 km cycling TTs; 1 and 2) ride-alone baseline TTs where a fastest baseline (FBL) performance was identified, 3) a TT against a virtual avatar representing 102% of their FBL performance (PACER), and 4) a subsequent ride-alone TT (SUB). The deception group, however, were initially informed that the avatar accurately represented their FBL, but prior to SUB were correctly informed of the nature of the avatar. Affect, self-efficacy and RPE were measured every quartile. Both groups performed PACER faster than FBL and SUB (p < 0.05) and experienced lower affect (p = 0.016), lower self-efficacy (p = 0.011), and higher RPE (p < 0.001) in PACER than FBL. No significant differences were found between FBL and SUB for any variable. The presence of the pacer rather than the manipulation of performance beliefs acutely facilitates TT performance and perceptual responses. Revealing that athletes’ performance beliefs were falsely negative due to deceptive feedback provision has no effect on subsequent perceptions or performance. A single experiential exposure may not be sufficient to produce meaningful changes in the performance beliefs of trained individuals beyond the acute setting

    Responses to 10 common criticisms of anti-racism action in STEMM

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    The wrongful murders of Black individuals during 2020 (including George Floyd, Breonna Taylor, Ahmaud Aubery, and others), compounded by a long history of similar incidents, inspired protests around the world against racism and police brutality. The growing anti-racism movement sparked conversations within science, technology, engineering, mathematics, and medicine (STEMM) surrounding ways to combat racial bias in our respective fields. A spotlight was placed on the discriminatory history of scientific research and medical practice, as well as the problematic modern-day policies that perpetuate the lack of racial diversity and equity in STEMM. While observing and participating in recent discussions about the racism that pervades institutions, departments, and scientific discourse, we have noticed a set of standard arguments against anti-racism action within STEMM. Ten of these arguments are laid out in this manuscript and paired with evidence-based counterarguments. Notably, while this manuscript is primarily centered around a United States perspective, most of our arguments and suggested actions remain applicable to other countries as well. It is crucial for a STEMM anti-racism movement to extend beyond national borders, reflecting the international nature of scientific research and collaboration. This team of authors represents a collaboration between scientists from historically marginalized groups and their allies. By compiling published academic literature, we hope to directly confront racist ideology in STEMM with evidence-based arguments while simultaneously amplifying the research and perspectives of scholars of color. Our broad goal in articulating this information is to facilitate more productive conversations (and, in turn, tangible systemic changes) toward addressing racial discrimination within STEMM

    The physiological roles of amyloid-beta peptide hint at new ways to treat Alzheimer&#039;s disease

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    Amyloid-beta (A beta) is best known as the misfolded peptide that is involved in the pathogenesis of Alzheimer&#039;s disease (AD), and it is currently the primary therapeutic target in attempts to arrest the course of this disease. This notoriety has overshadowed evidence that A beta serves several important physiological functions. A beta is present throughout the lifespan, it has been found in all vertebrates examined thus far, and its molecular sequence shows a high degree of conservation. These features are typical of a factor that contributes significantly to biological fitness, and this suggestion has been supported by evidence of functions that are beneficial for the brain. The putative roles of A beta include protecting the body from infections, repairing leaks in the blood-brain barrier, promoting recovery from injury, and regulating synaptic function. Evidence for these beneficial roles comes from in vitro and in vivo studies, which have shown that the cellular production of A beta rapidly increases in response to a physiological challenge and often diminishes upon recovery. These roles are further supported by the adverse outcomes of clinical trials that have attempted to deplete A beta in order to treat AD. We suggest that anti-A beta therapies will produce fewer adverse effects if the known triggers of A beta deposition (e.g., pathogens, hypertension, and diabetes) are addressed first
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