Automatic Registration of Footsteps in Contact Regions for Reactive Agility Training in Sports.

In collective sports, reactive agility training methodologies allow to evaluate and improve the player performance, being able to consider a mixture of technical, tactical, physical, and psychological abilities, similarly to real game-play situations. In this article, we present a new methodology for reactive agility training (neural training), the technological setup for the methodology, and a new footstep tracking algorithm, as the key element for automating the speed data gathering process, necessary for obtaining the relevant variables of the neural training approach. This new methodology is oriented to accurately measure two of the most relevant variables for reactive agility training: total response time (sprint time) and response correctness, related to a stimuli sequence presented to a player. The stimuli were designed to properly represent realistic competitive conditions for player training, contextualized to soccer. In order to automate the gathering process, a new computer vision based automatic footstep detection algorithm has been integrated to the system. The algorithm combines Kalman Filters, segmentation techniques, and perspective geometry, for obtaining highly precise detections of the moment a relevant footstep occurs in real-time, reaching a precision higher than 97%. Plus, the algorithm does not require any special marker, invasive sensor, or clothing constraint on the player.

Endothelin-1 decreases ethanolamine plasmalogen levels and evokes PAF production in brain microvessels.

Treatment of brain microvessels with Endothelin-1 evoked a decrease in ethanolamine plasmalogen levels by calcium-independent phospholipase A(2). In contrast, the diacyl molecular forms of ethanolamine phospholipids were unaffected. Evidence also shows that Endothelin type A receptors are involved. Concomitantly, PAF production mediated by CoA-independent transacylase was observed. This is the first evidence of involvement of these pathways on the Endothelin-1 mechanism of action on the blood-brain barrier.

Brain microvessel endothelin type A receptors are coupled to ceramide production.

Treatment of brain microvessels with endothelin-1 evoked an early decrease in the sphingomyelin levels concomitantly with an increase in those of ceramides. These responses were time- and concentration-dependent. Evidence also shows that endothelin type A receptors are involved. This is the first report on the involvement of an agonist in the regulation of the ceramide signal transduction system on blood-brain barrier and shows a new pathway likely involved in the regulation of the cerebral microvascular functioning.

Signaling events mediating activation of brain ethanolamine plasmalogen hydrolysis by ceramide.

Ceramide is a lipid second messenger that acts on multiple-target enzymes, some of which are involved in other signal-transduction systems. We have previously demonstrated that endogenous ceramide modifies the metabolism of brain ethanolamine plasmalogens. The mechanism involved was studied. On the basis of measurements of breakdown products, specific inhibitor effects, and previous findings, we suggest that a plasmalogen-selective phospholipase A2 is the ceramide target. Arachidonate-rich pools of the diacylphosphatidylethanolamine subclass were also affected by ceramide, but the most affected were plasmalogens. Concomitantly with production of free arachidonate, increased 1-O-arachidonoyl ceramide formation was observed. Quinacrine (phospholipase A2 inhibitor) and 1-O-octadecyl-2-O-methyl-rac-glycerol-3-phosphocholine (CoA-independent transacylase inhibitor) prevented all of these ceramide-elicited effects. Therefore, phospholipase and transacylase activities are tightly coupled. Okadaic acid (phosphatase 2A inhibitor) and PD 98059 (mitogen-activated protein kinase inhibitor) modified basal levels of ceramide and sphingomyelinase-induced accumulation of ceramide, respectively. Therefore, they provided no evidence to determine whether there is a sensitive enzyme downstream of ceramide. The evidence shows that there are serine-dependent and thiol-dependent enzymes downstream of ceramide generation. Furthermore, experiments with Ac-DEVD-CMK (caspase-3 specific inhibitor) have led us to conclude that caspase-3 is downstream of ceramide in activating the brain plasmalogen-selective phospholipase A2.

Exercise training-induced changes in sensitivity to endothelin-1 and aortic and cerebellum lipid profile in rats.

The purpose of this work was to study whether exercise training induces changes in the lipid profile of rat aorta and nervous system and in the in vitro intrinsic responsiveness of these tissues to endothel in-1 (ET-1) treatment. The exercise program performed successfully produced the characteristic metabolic alterations of the trained state. Exercise training induced a large and significant increase in the levels of both aortic ethanolamine plasmalogens (PlasEtn) and glucosylceramides. In contrast, a decrease of aortic ceramide and cholesterol levels was evoked by exercise training. ET-1 increased PlasEtn content only in sedentary animals. An exercise-induced increase in cerebellum levels of ceramides and ceramide monohexosides was found. The cerebellum ceramide content was increased by ET-1 more noticeably in sedentary rats than in trained animals. In contrast, cerebral cortex was observed to be largely insensitive to both exercise training and ET-1 treatment. It was concluded that exercise training (i) induces changes in both vascular and cerebellar lipid profiles, the former being much more pronounced than the latter, and (ii) diminishes the aortic and cerebellar sensitivity to ET-1 action.