Flow Visualization of Downhill Ski Racers Using Computational Fluid Dynamics

AbstractIn downhill alpine skiing, racers often exceed speeds of 120km/h, with air resistance substantially affecting the overall race times. To date, studies on air resistance in alpine skiing have used wind tunnels and actual skiers to examine the relationship between the gliding posture and magnitude of drag, as well as for the design of skiing equipment. However, these studies have not revealed the flow velocity distribution and vortex structure around the skier. In the present study, we used computational fluid dynamics with the lattice Boltzmann method to derive the relationship between flow velocity in the full tuck position (the downhill racer's speed) and total drag. Furthermore, we visualized the flow around the downhill racer and examined its vortex structure. The results show that the total drag force in the downhill racer model is 27.0N at a flow velocity of 15 m/s, increasing to 185.8N at 40 m/s. Moreover, the visualization of the flow field indicates that the primary drag locations at a flow velocity of 40 m/s are the head, upper arms, lower legs, and thighs (including the buttocks)

SKIP Negatively Regulates Insulin-Induced GLUT4 Translocation and Membrane Ruffle Formation

Skeletal muscle and kidney enriched inositol phosphatase (SKIP) is an inositol polyphosphate 5-phosphatase that hydrolyzes phosphatidylinositol 3,4,5-trisphosphate [PI(3,4,5)P(3)] to downregulate intracellular levels. In this study, we show that SKIP inhibits phosphoinositide 3-kinase signaling in insulin-stimulated CHO cells. Ectopic expression of SKIP did not inhibit insulin-induced PI(3,4,5)P(3) generation but did rapidly decrease insulin-induced intracellular PI(3,4,5)P(3) levels compared with those in control cells. Further, insulin-induced phosphorylation of some downstream targets such as Akt and p70 S6 kinase was markedly inhibited by the ectopic expression of SKIP, whereas phosphorylation of mitogen-activated protein kinase was not. In contrast, downregulation of intracellular SKIP levels by antisense oligonucleotides dramatically enhanced Akt (protein kinase B) phosphorylation in response to insulin, suggesting that endogenous SKIP downregulates insulin signaling. SKIP also markedly inhibited GLUT4 translocation and membrane ruffle formation. We conclude that SKIP preferentially regulates glucose transport and actin cytoskeletal rearrangement among a variety of PI(3,4,5)P(3) downstream events