Appropriate Loads for Peak-Power During Resisted Sprinting on a Non-Motorized Treadmill

The purpose of this study was to determine the load which allows the highest peak power for resisted sprinting on a non-motorized treadmill and to determine if other variables are related to individual differences. Thirty college students were tested for vertical jump, vertical jump peak and mean power, 10 m sprint, 20 m sprint, leg press 1 RM, leg press 1 RM relative to body weight, leg press 1 RM relative to lean body mass, leg press 1 RM power, and leg press power at 80% of 1 RM. Participants performed eight resisted sprints on a non-motorized treadmill, with increasing relative loads expressed as percent of body weight. Sprint peak power was measured for each load. Pearson correlations were used to determine if relationships between the sprint peak power load and the other variables were significant. The sprint peak power load had a mode of 35% with 73% of all participants having a relative sprint peak power load between 25-35%. Significant correlations occurred between sprint peak power load and body weight, lean body mass, vertical jump peak and mean power, leg press 1 RM, leg press 1 RM relative to lean body mass, leg press 1 RM power, and leg press power at 80% of 1 RM (r = 0.44, 0.43, 0.39, 0.37, 0.47, 0.39, 0.46, and 0.47, respectively). Larger, stronger, more powerful athletes produced peak power at a higher relative load during resisted sprinting on a nonmotorized treadmill

VALIDATION OF A 3-DIMENSIONAL VIDEO MOTION CAPTURE SYSTEM FOR DETERMINING BARBELL POWER AND VELOCITY DURING THE BENCH PRESS

Andrew C. Fry, Luke Bradford, Trent Herda, Joseph Weir FACSM, Michael Lane, Matthew Andre, Andrea Hudy, J. Deckert and J. Siedlik.Neuromechanics Laboratory and Kansas Athletics Inc., University of Kansas, Lawrence, KS Analyses of barbell kinetics and kinematics have typically required the use of force plates, tether-based position transducers, or digitized video analysis. PURPOSE: To determine the validity of a 3-dimensional video markerless motion capture system for determining barbell kinetics and kinematics. METHODS: Two 3-D video cameras sampling at 30 Hz and mounted on the top of a power rack were interfaced with a self-contained computer and software system, and operated with a touch screen (EliteForm, Lincoln, NE). For laboratory comparison purposes, a ceiling–mounted linear position transducer (Unimeasure, Corvallis, OR) was attached via a tether to the barbell. Data from the position transducer was sampled at 1000 Hz using a BioPac data acquisition system (Goleta, CA). Velocity (m.s-1) and power (W) were derived using LabView software (National Instruments, Austin, TX). One weight-trained male subject (age = 25 yrs, hgt = 1.75 m, BW = 82.6 kg, 1 RM = 161.0 kg) performed the barbell bench press exercise for 10 sets x 1 repetition at 30, 40, 50, 60, 70 and 80% 1 RM loads using maximal acceleration during the concentric phase. Dependent variables included peak (PV) and X̅ velocity (MV) and peak (PP) and X̅ power (MP). Linear regressions between lab-derived and 3-D video-derived data provided correlation coefficients, and regression slopes (b). Bland-Altman plots were used to determine X̅ differences, from which effect sizes (Cohen’s D) and % error for the 3-D camera system was determined. RESULTS: Lab-derived mean values for all loads ranged as follows; MV = 0.36 – 1.00 m.s-1, PV = 0.47 – 1.60 m.s-1, MP = 460.9 – 621.6 W, and PP = 619.9 – 1055.6 W. CONCLUSION: The 3-D video markerless motion capture system provided accurate and valid barbell velocity and power data for the bench press exercise. Supported in part by Nebraska Global LL

Endocrine responses and acute mTOR pathway phosphorylation to resistance exercise with leucine and whey

Leucine ingestion reportedly activates the mTOR pathway in skeletal muscle, contributing to a hypertrophy response. The purpose of the study was to compare the post-resistance exercise effects of leucine and whey protein supplementation on endocrine responses and muscle mTOR pathway phosphorylation. On visit 1, subjects (X±SD; n=20; age=27.8±2.8yrs) provided baseline blood samples for analysis of cortisol, glucose and insulin; a muscle biopsy of the vastus lateralis muscle to assess mTOR signaling pathway phosphorylation; and were tested for maximum strength on the leg press and leg extension exercises. For visits 2 and 3, subjects were randomized in a double-blind crossover design to ingest either leucine and whey protein (10g+10g; supplement) or a non-caloric placebo. During these visits, 5 sets of 10 repetitions were performed on both exercises, immediately followed by ingestion of the supplement or placebo. Blood was sampled 30 min post-, and a muscle biopsy 45 min post-exercise. Western blots quantified total and phosphorylated proteins. Insulin increased (α<.05) with supplementation with no change in glucose compared to placebo. Relative phosphorylation of AKT and rpS6 were greater with leucine and whey supplementation compared to placebo. Supplementation of leucine and whey protein immediately after heavy resistance exercise increases anabolic signaling in human skeletal muscle

OH-Stretch Vibrational Spectroscopy of Hydroxymethyl Hydroperoxide

We report measurement and analysis of the photodissociation spectrum of hydroxymethyl hydroperoxide (HOCH_2OOH) and its partially deuterated analogue, HOCD_2OOH, in the OH-stretching region. Spectra are obtained by Fourier transform infrared spectroscopy in the 1ν_(OH) and 2ν_(OH) regions, and by laser induced fluorescence detection of the OH fragment produced from dissociation of HOCH_2OOH initiated by excitation of the 4ν_(OH) and 5ν_(OH) overtone regions (action spectroscopy). A one-dimensional local-mode model of each OH chromophore is used with ab initio calculated OH-stretching potential energy and dipole moment curves at the coupled-cluster level of theory. Major features in the observed absorption and photodissociation spectra are explained by our local-mode model. In the 4ν_(OH) region, explanation of the photodissocation spectrum requires a nonuniform quantum yield, which is estimated by assuming statistical energy distribution in the excited state. Based on the estimated dissociation threshold, overtone photodissociation is not expected to significantly influence the atmospheric lifetime of hydroxymethyl hydroperoxide

The Centrosomal Protein C-Nap1 Is Required for Cell Cycle–Regulated Centrosome Cohesion

Duplicating centrosomes are paired during interphase, but are separated at the onset of mitosis. Although the mechanisms controlling centrosome cohesion and separation are important for centrosome function throughout the cell cycle, they remain poorly understood. Recently, we have proposed that C-Nap1, a novel centrosomal protein, is part of a structure linking parental centrioles in a cell cycle–regulated manner. To test this model, we have performed a detailed structure–function analysis on C-Nap1. We demonstrate that antibody-mediated interference with C-Nap1 function causes centrosome splitting, regardless of the cell cycle phase. Splitting occurs between parental centrioles and is not dependent on the presence of an intact microtubule or microfilament network. Centrosome splitting can also be induced by overexpression of truncated C-Nap1 mutants, but not full-length protein. Antibodies raised against different domains of C-Nap1 prove that this protein dissociates from spindle poles during mitosis, but reaccumulates at centrosomes at the end of cell division. Use of the same antibodies in immunoelectron microscopy shows that C-Nap1 is confined to the proximal end domains of centrioles, indicating that a putative linker structure must contain additional proteins. We conclude that C-Nap1 is a key component of a dynamic, cell cycle–regulated structure that mediates centriole–centriole cohesion

Pectic polysaccharides are attacked by hydroxyl radicals in ripening fruit: evidence from a fluorescent fingerprinting method

Background and aims Many fruits soften during ripening, which is important commercially and in rendering the fruit attractive to seed-dispersing animals. Cell-wall polysaccharide hydrolases may contribute to softening, but sometimes appear to be absent. An alternative hypothesis is that hydroxyl radicals ((•)OH) non-enzymically cleave wall polysaccharides. We evaluated this hypothesis by using a new fluorescent labelling procedure to ‘fingerprint’ (•)OH-attacked polysaccharides. Methods We tagged fruit polysaccharides with 2-(isopropylamino)-acridone (pAMAC) groups to detect (a) any mid-chain glycosulose residues formed in vivo during (•)OH action and (b) the conventional reducing termini. The pAMAC-labelled pectins were digested with Driselase, and the products resolved by high-voltage electrophoresis and high-pressure liquid chromatography. Key Results Strawberry, pear, mango, banana, apple, avocado, Arbutus unedo, plum and nectarine pectins all yielded several pAMAC-labelled products. GalA–pAMAC (monomeric galacturonate, labelled with pAMAC at carbon-1) was produced in all species, usually increasing during fruit softening. The six true fruits also gave pAMAC·UA-GalA disaccharides (where pAMAC·UA is an unspecified uronate, labelled at a position other than carbon-1), with yields increasing during softening. Among false fruits, apple and strawberry gave little pAMAC·UA-GalA; pear produced it transiently. Conclusions GalA–pAMAC arises from pectic reducing termini, formed by any of three proposed chain-cleaving agents ((•)OH, endopolygalacturonase and pectate lyase), any of which could cause its ripening-related increase. In contrast, pAMAC·UA-GalA conjugates are diagnostic of mid-chain oxidation of pectins by (•)OH. The evidence shows that (•)OH radicals do indeed attack fruit cell wall polysaccharides non-enzymically during softening in vivo. This applies much more prominently to drupes and berries (true fruits) than to false fruits (swollen receptacles). (•)OH radical attack on polysaccharides is thus predominantly a feature of ovary-wall tissue

C-Nap1, a Novel Centrosomal Coiled-Coil Protein and Candidate Substrate of the Cell Cycle–regulated Protein Kinase Nek2

Nek2 (for NIMA-related kinase 2) is a mammalian cell cycle–regulated kinase structurally related to the mitotic regulator NIMA of Aspergillus nidulans. In human cells, Nek2 associates with centrosomes, and overexpression of active Nek2 has drastic consequences for centrosome structure. Here, we describe the molecular characterization of a novel human centrosomal protein, C-Nap1 (for centrosomal Nek2-associated protein 1), first identified as a Nek2-interacting protein in a yeast two-hybrid screen. Antibodies raised against recombinant C-Nap1 produced strong labeling of centrosomes by immunofluorescence, and immunoelectron microscopy revealed that C-Nap1 is associated specifically with the proximal ends of both mother and daughter centrioles. On Western blots, anti–C-Nap1 antibodies recognized a large protein (>250 kD) that was highly enriched in centrosome preparations. Sequencing of overlapping cDNAs showed that C-Nap1 has a calculated molecular mass of 281 kD and comprises extended domains of predicted coiled-coil structure. Whereas C-Nap1 was concentrated at centrosomes in all interphase cells, immunoreactivity at mitotic spindle poles was strongly diminished. Finally, the COOH-terminal domain of C-Nap1 could readily be phosphorylated by Nek2 in vitro, as well as after coexpression of the two proteins in vivo. Based on these findings, we propose a model implicating both Nek2 and C-Nap1 in the regulation of centriole–centriole cohesion during the cell cycle

The northern Hikurangi margin three-dimensional plate interface in New Zealand remains rough 100 km from the trench

At the northern Hikurangi margin (North Island, New Zealand), shallow slow slip events (SSEs) frequently accommodate subduction-interface plate motion from landward of the trench to <20 km depth. SSEs may be spatially related to geometrical interface heterogeneity, though kilometer-scale plate-interface roughness imaged by active-source seismic methods is only constrained offshore at <12 km depth. Onshore constraints are comparatively lacking, but we mapped the Hikurangi margin plate interface using receiver functions from data collected by a dense 22 × 10 km array of 49 broadband seismometers. The plate interface manifests as a positive-amplitude conversion (velocity increase with depth) dipping west from 10 to 17 km depth. This interface corroborates relocated earthquake hypocenters, seismic velocity models, and downdip extrapolation of depth-converted two-dimensional active-source lines. Our mapped plate interface has kilometer-amplitude roughness we interpret as oceanic volcanics or seamounts, and is 1–4 km shallower than the regional-scale plate-interface model used in geodetic inversions. Slip during SSEs may thus have different magnitudes and/or distributions than previously thought. We show interface roughness also leads to shear-strength variability, where slip may nucleate in locally weak areas and propagate across areas of low shear-strength gradient. Heterogeneous shear strength throughout the depth range of the northern Hikurangi margin may govern the nature of plate deformation, including the localization of both slow slip and hazardous earthquakes

The northern Hikurangi margin three-dimensional plate interface in New Zealand remains rough 100 km from the trench

At the northern Hikurangi margin (North Island, New Zealand), shallow slow slip events (SSEs) frequently accommodate subduction-interface plate motion from landward of the trench to <20 km depth. SSEs may be spatially related to geometrical interface heterogeneity, though kilometer-scale plate-interface roughness imaged by active-source seismic methods is only constrained offshore at <12 km depth. Onshore constraints are comparatively lacking, but we mapped the Hikurangi margin plate interface using receiver functions from data collected by a dense 22 × 10 km array of 49 broadband seismometers. The plate interface manifests as a positive-amplitude conversion (velocity increase with depth) dipping west from 10 to 17 km depth. This interface corroborates relocated earthquake hypocenters, seismic velocity models, and downdip extrapolation of depth-converted two-dimensional active-source lines. Our mapped plate interface has kilometer-amplitude roughness we interpret as oceanic volcanics or seamounts, and is 1–4 km shallower than the regional-scale plate-interface model used in geodetic inversions. Slip during SSEs may thus have different magnitudes and/or distributions than previously thought. We show interface roughness also leads to shear-strength variability, where slip may nucleate in locally weak areas and propagate across areas of low shear-strength gradient. Heterogeneous shear strength throughout the depth range of the northern Hikurangi margin may govern the nature of plate deformation, including the localization of both slow slip and hazardous earthquakes