论文标题
高雷诺数中的涡流拉伸和肠病产生数量湍流
Vortex stretching and enstrophy production in high Reynolds number turbulence
论文作者
论文摘要
湍流的基本要素是涡旋拉伸机制,它是由涡度和应变率张量的非线性相互作用所散发的,并导致形成极端事件。我们通过使用从周期域中强迫各向同性湍流的非常完善的直接数值模拟产生的大量数据库来分析涡度和应变速率之间的统计相关性。电网分辨率高达$ 12288^3 $,泰勒级雷诺数的编号为$ 140-1300 $。为了理解极端涡度波动的形成和结构,我们获得了以endrophophy为条件的统计数据(涡旋方相)。当在弱肠子卵形上调节时,应变的大小及其特征值大约是恒定的。尽管它们大约是作为强大的肠道的力量定律而生长的,但随着$r_λ$的增加,它们变得更加陡峭。我们发现,涡度张量的涡度和中间特征向量之间的众所周知的优惠对准对于大型腹部而言甚至更强,而涡度显示出对最广泛的特征向量(对于大型腹部)而言是弱正交的趋势。然而,最广泛的特征是对大型腹部事件产生的主要贡献,随着$r_λ$的增加,越来越多。然而,强烈的涡度区域的拉伸显着耗尽,这与它们组织的弱弯曲管的运动学特性一致。进一步的分析表明,尽管粘性耗散也很明显,但强烈的腹膜植物主要是通过粘性扩散耗尽的。名义上解决了对建模的影响。
An essential ingredient of turbulent flows is the vortex stretching mechanism, which emanates from the non-linear interaction of vorticity and strain-rate tensor and leads to formation of extreme events. We analyze the statistical correlations between vorticity and strain rate by using a massive database generated from very well resolved direct numerical simulations of forced isotropic turbulence in periodic domains. The grid resolution is up to $12288^3$, and the Taylor-scale Reynolds number is in the range $140-1300$. In order to understand the formation and structure of extreme vorticity fluctuations, we obtain statistics conditioned on enstrophy (vorticity-squared). The magnitude of strain, as well as its eigenvalues, is approximately constant when conditioned on weak enstrophy; whereas they grow approximately as power laws for strong enstrophy, which become steeper with increasing $R_λ$. We find that the well-known preferential alignment between vorticity and the intermediate eigenvector of strain tensor is even stronger for large enstrophy, whereas vorticity shows a tendency to be weakly orthogonal to the most extensive eigenvector (for large enstrophy). Yet the dominant contribution to the production of large enstrophy events arises from the most extensive eigendirection, the more so as $R_λ$ increases. Nevertheless, the stretching in intense vorticity regions is significantly depleted, consistent with the kinematic properties of weakly-curved tubes in which they are organized. Further analysis reveals that intense enstrophy is primarily depleted via viscous diffusion, though viscous dissipation is also significant. Implications for modeling are nominally addressed as appropriate.