Performance Motion Analysis Unable to Predict Running-Related Injury in Collegiate Distance Runners

ABSTRACT Purpose: Running-related injury (RRI) is common among competitive collegiate distance runners who participate in the sport of cross country and long distance track and field. Many factors contribute to RRI. Therefore, the purpose of this study was to determine if a 3D motion capture system’s performance motion analysis (PMA) report is capable of identifying factors predictive of RRI among collegiate distance runners during a cross country season. Methods: Thirty-one collegiate cross country runners (17 male, 14 female, mean age = 20.5 ± 1.4 years) gave their consent to participate in the investigation. Subjects were screened in the motion capture system and provided with PMA reports assessing their movement quality using several variables (composite score, power, strength, dysfunction, and vulnerability, based on measurements of 192 kinetic and kinematic variables). The athletes were then monitored throughout their 13-week competitive season for incidence of RRI. At the end of the season, participants were sorted into injured (n=17) and uninjured (n=14) groups. Injury was defined as appearing on the team injury report as missing or being limited in practice or competition for a week or more, in accordance with prior RRI research. Each sex was also separated into groups based on injury status. Results: Independent samples t-tests (pConclusion: The findings identified in this prospective study suggest that the movement screen was unable to identify runners at risk of injury. Future investigations isolating lower extremity movement characteristics in runners may prove more effective at predicting RRI

Ascorbate degradation: pathways, products and possibilities

A role for l-ascorbate as the precursor of several plant compounds adds to its already broad metabolic utility. There are many examples of plant species in which oxalate and l-threonate are formed from l-ascorbate breakdown, and a number of roles have been proposed for this: structural, physiological, and biochemical. On the other hand, the synthesis of l-tartrate from l-ascorbate remains limited to a very few species, amongst which we must be grateful to count the domesticated grapevine Vitis vinifera and its relatives on which wine production is based. Pathways for the degradation of ascorbate were first proposed ~50 years ago and have formed the basis of more recent biochemical and molecular analyses. The present review seeks to summarize some of these findings and to propose opportunities for future research.</p

Geodatabase Development to Support Hyperspectral Imagery Exploitation

Geodatabase development for coastal studies conducted by the Naval Research Laboratory (NRL) is essential to support the exploitation of hyperspectral imagery (HSI). NRL has found that the remote sensing and mapping science community benefits from coastal classifications that group coastal types based on similar features. Selected features in project geodatabases relate to significant biological and physical forces that shape the coast. The project geodatabases help researchers understand factors that are necessary for imagery post processing, especially those features having a high degree of temporal and spatial variability. NRL project geodatabases include a hierarchy of environmental factors that extend from shallow water bottom types and beach composition to inland soil and vegetation characteristics. These geodatabases developed by NRL allow researchers to compare features among coast types. The project geodatabases may also be used to enhance littoral data archives that are sparse. This paper highlights geodatabase development for recent remote sensing experiments in barrier island, coral, and mangrove coast types

Emphasizing Task-Specific Hypertrophy to Enhance Sequential Strength and Power Performance

While strength is indeed a skill, most discussions have primarily considered structural adaptations rather than ultrastructural augmentation to improve performance. Altering the structural component of the muscle is often the aim of hypertrophic training, yet not all hypertrophy is equal; such alterations are dependent upon how the muscle adapts to the training stimuli and overall training stress. When comparing bodybuilders to strength and power athletes such as powerlifters, weightlifters, and throwers, while muscle size may be similar, the ability to produce force and power is often inequivalent. Thus, performance differences go beyond structural changes and may be due to the muscle’s ultrastructural constituents and training induced adaptations. Relative to potentiating strength and power performances, eliciting specific ultrastructural changes should be a variable of interest during hypertrophic training phases. By focusing on task-specific hypertrophy, it may be possible to achieve an optimal amount of hypertrophy while deemphasizing metabolic and aerobic components that are often associated with high-volume training. Therefore, the purpose of this article is to briefly address different types of hypertrophy and provide directions for practitioners who are aiming to achieve optimal rather than maximal hypertrophy, as it relates to altering ultrastructural muscular components, to potentiate strength and power performance

Emphasizing Task-Specific Hypertrophy to Enhance Sequential Strength and Power Performance

While strength is indeed a skill, most discussions have primarily considered structural adaptations rather than ultrastructural augmentation to improve performance. Altering the structural component of the muscle is often the aim of hypertrophic training, yet not all hypertrophy is equal; such alterations are dependent upon how the muscle adapts to the training stimuli and overall training stress. When comparing bodybuilders to strength and power athletes such as powerlifters, weightlifters, and throwers, while muscle size may be similar, the ability to produce force and power is often inequivalent. Thus, performance differences go beyond structural changes and may be due to the muscle’s ultrastructural constituents and training induced adaptations. Relative to potentiating strength and power performances, eliciting specific ultrastructural changes should be a variable of interest during hypertrophic training phases. By focusing on task-specific hypertrophy, it may be possible to achieve an optimal amount of hypertrophy while deemphasizing metabolic and aerobic components that are often associated with high-volume training. Therefore, the purpose of this article is to briefly address different types of hypertrophy and provide directions for practitioners who are aiming to achieve optimal rather than maximal hypertrophy, as it relates to altering ultrastructural muscular components, to potentiate strength and power performance

Regulation of gap junction conductance by calcineurin through Cx43 phosphorylation: implications for action potential conduction

Cardiac arrhythmias are associated with raised intracellular [Ca2+] and slowed action potential conduction caused by reduced gap junction (GJ) electrical conductance (Gj). Ventricular GJs are composed of connexin proteins (Cx43), with Gj determined by Cx43 phosphorylation status. Connexin phosphorylation is an interplay between protein kinases and phosphatases but the precise pathways are unknown. We aimed to identify key Ca2+-dependent phosphorylation sites on Cx43 that regulate cardiac gap junction conductance and action potential conduction velocity. We investigated the role of the Ca2+-dependent phosphatase, calcineurin. Intracellular [Ca2+] was raised in guinea-pig myocardium by a low-Na solution or increased stimulation. Conduction velocity and Gj were measured in multicellular strips. Phosphorylation of Cx43 serine residues (S365 and S368) and of the intermediary regulator I1 at threonine35 was measured by Western blot. Measurements were made in the presence and absence of inhibitors to calcineurin, I1 or protein phosphatase-1 and phosphatase-2. Raised [Ca2 +]i decreased Gj, reduced Cx43 phosphorylation at S365 and increased it at S368; these changes were reversed by calcineurin inhibitors. Cx43-S368 phosphorylation was reversed by the protein kinase C inhibitor chelerythrine. Raised [Ca2+]i also decreased I1 phosphorylation, also prevented by calcineurin inhibitors, to increase activity of the Ca2+-independent phosphatase, PPI. The PP1 inhibitor, tautomycin, prevented Cx43-365 dephosphorylation, Cx43-S368 phosphorylation and Gj reduction in raised [Ca2+]i. PP2A had no role. Conduction velocity was reduced by raised [Ca2+]i and reversed by calcineurin inhibitors. Reduced action potential conduction and Gj in raised [Ca2+] are regulated by calcineurin-dependent Cx43-S365 phosphorylation, leading to Cx43-S368 dephosphorylation. The calcineurin action is indirect, via I1 dephosphorylation and subsequent activation of PP1.Centro de Investigaciones Cardiovasculare

Muscle fiber and performance adaptations to resistance exercise with MyoVive, colostrum or casein and whey supplementationa

This is the publisher's version, also found at http://ehis.ebscohost.com/ehost/detail?sid=ba69ee0d-97cf-4a2c-a1a2-2c26fb60d65c%40sessionmgr13&vid=1&hid=2&bdata=JnNpdGU9ZWhvc3QtbGl2ZQ%3d%3d#db=s3h&AN=10725638To determine the effects of 12 weeks of resistance exercise with MyoVive and/or colostrum supplementation, 19 male and female recreationally weighttrained subjects (X ± SE; age = 28.3 ± 6.9 yrs; hgt = 68.2 ± 3.8 cm) were divided into MyoVive + colostrum (n = 4), MyoVive + casein & whey (n = 4), colostrum + casein & whey (n = 6), and casein & whey (n = 5) groups. All groups similarly increased (p < .05) 1 repetition maximum (RM) leg press (kg; pre = 158.6 ± 12.8, post = 189.3 ± 11.3), body mass (kg; pre = 79.0 ± 3.2, post = 80.7 ± 3.8), and lean body mass (kg; pre = 60.1 ± 3.1, post = 62.2 ± 2.8). Increases were observed for peak force (N; all loads), peak velocity (m.s-1; 70% & 40% 1 RM), and peak power (W; 70% & 40% 1 RM) for all groups for the leg press exercise, with no differences between groups. When performance data were adjusted for body mass, lean body mass, lower body lean mass as determined by DEXA, or % change, no group differences were observed. Relative (%) fiber type content, cross-sectional areas (mm2), % fiber type areas, or % myosin heavy chain expression did not change for any group. These data suggest that MyoVive and colostrum supplementation have no greater effect on cellular and performance adaptations when compared to casein and whey protein

Regulation of gap junction conductance by calcineurin through Cx43 phosphorylation: implications for action potential conduction.

Cardiac arrhythmias are associated with raised intracellular [Ca2+] and slowed action potential conduction caused by reduced gap junction (GJ) electrical conductance (Gj). Ventricular GJs are composed of connexin proteins (Cx43), with Gj determined by Cx43 phosphorylation status. Connexin phosphorylation is an interplay between protein kinases and phosphatases but the precise pathways are unknown. We aimed to identify key Ca2+-dependent phosphorylation sites on Cx43 that regulate cardiac gap junction conductance and action potential conduction velocity. We investigated the role of the Ca2+-dependent phosphatase, calcineurin. Intracellular [Ca2+] was raised in guinea-pig myocardium by a low-Na solution or increased stimulation. Conduction velocity and Gj were measured in multicellular strips. Phosphorylation of Cx43 serine residues (S365 and S368) and of the intermediary regulator I1 at threonine35 was measured by Western blot. Measurements were made in the presence and absence of inhibitors to calcineurin, I1 or protein phosphatase-1 and phosphatase-2.Raised [Ca2+]i decreased Gj, reduced Cx43 phosphorylation at S365 and increased it at S368; these changes were reversed by calcineurin inhibitors. Cx43-S368 phosphorylation was reversed by the protein kinase C inhibitor chelerythrine. Raised [Ca2+]i also decreased I1 phosphorylation, also prevented by calcineurin inhibitors, to increase activity of the Ca2+-independent phosphatase, PPI. The PP1 inhibitor, tautomycin, prevented Cx43-365 dephosphorylation, Cx43-S368 phosphorylation and Gj reduction in raised [Ca2+]i. PP2A had no role. Conduction velocity was reduced by raised [Ca2+]i and reversed by calcineurin inhibitors. Reduced action potential conduction and Gj in raised [Ca2+] are regulated by calcineurin-dependent Cx43-S365 phosphorylation, leading to Cx43-S368 dephosphorylation. The calcineurin action is indirect, via I1 dephosphorylation and subsequent activation of PP1